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HEALTH 
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DISEASES  OF  THE  CHEST 

AND  THE  PRINCIPLES  OF 

PHYSICAL  DIAGNOSIS^ 

f 


BY 

GEORGE  WILLIAM  NORMS,  A.  B.,  M.  D. 

Assistant  Professor  of  Medicine  in  the  University  of  Pennsylvania;  Visiting  Physician 
to  the  Pennsylvania  Hospital;  Assistant  Visiting  Physician  to  the  University  Hospital 

AND 

HENRY  R.  M.  LANDIS,  A.  B.,  M.  D. 

Assistant  Professor  of   Medicine  in  the   University  of  Pennsylvania;    Director  of  the 

Clinical  and  Sociological  Departments  of  the  Henry  Phipps  Institute  of  the  University 

of  Pennsylvania;  Visiting  Physician  to  the  White  Haven  Sanatorium 


WITH  A  CHAPTER  ON  THE 

ELECTROCARDIOGRAPH  IN  HEART  DISEASE 

BY 

EDWARD  B.  KRUMBHAAR,  Ph.D.,  M.  D. 

Assistant  Professor  of  Research  Medicine  in  the  University  of  Pennsylvania 


PHILADELPHIA  AND  LONDON 

W.    B.    SAUNDERS    COMPANY 

1917 


Copyright,  1917,  by  W.  B.  Saunders  Company. 


Printed  in  America. 


DEDICATED  TO 
OUR  FRIEND 

GEORGE  FETTEROLF,  A.  B.,  M.  D.,  Sc.  D. 

ASSISTANT    PROFESSOR   OF    ANATOMY   IN   THE    UNIVERSITY    OF    PENNSYLVANIA 

TO    WHOM    WE    ARE   INDEBTED  FOR    MOST    OF  OUR    ANATOMIC    SECTIONS 

WITHOUT  WHOSE  CO-OPERATION,  CORDIAL  AND  SELF-EFFACING, 

OUR  BOOK   WOULD    LACK   WHAT   IS    PROBABLY    ITS 

MOST    CHARACTERISTIC    FEATURE. 


PREFACE 


To  write  a  practical  book  on  the  physical  diagnosis  of  the  heart  and 
lungs  in  health  and  disease,  has  been  the  aim  of  the  authors.  We  have  at- 
tempted to  omit  everything  not  of  practical  diagnostic  use,  and  to  con- 
dense methods  of  secondary  importance. 

More  than  is  the  custom  has  been  written  on  the  subject  of  diagnostic 
acoustics,  because  we  believe  that  only  through  the  comprehension  of  the 
laws  of  sound  production  and  transmission  can  the  results  of  percussion 
and  auscultation  be  intelligently  interpreted. 

We  have  endeavored  to  teach  as  much  as  possible  by  means  of  illus- 
trations. Of  these,  many  are  photographs  of  frozen  sections  from  the 
cadaver,  previously  hardened  in  formalin,  so  that  the  anatomic  relations 
of  the  tissues  remain  as  during  life.1  We  have  found  these  specimens 
invaluable  in  our  own  teaching;  and  the  book  has  been  written  in  the  hope 
that  the  photographic  reproductions  of  our  sections  may  be  useful  to 
others. 

We  take  pleasure  in  acknowledging  our  great  indebtedness  to  Dr. 
George  Fetterolf  for  the  frozen  sections;  to  Dr.  J.  Claxton  Gittings  for 
assistance  in  the  preparation  of  the  Section  on  Pediatrics;  to  Dr.  Edward 
B.  Krumbhaar  for  the  Chapter  dealing  with  the  electrocardiogram;  to 
Professor  Richard  Geigel,2  and  to  Dr.  Charles  M.  Montgomery,3 
from  whose  articles  upon  acoustics  in  diagnosis,  much  information  has 
been  gleaned.  We  are  also  indebted  to  Miss  Eleanor  A.  Cantner  for  the 
production  of  some  of  our  drawings.  We  are  further  under  obligations 
to  Professor  William  M.  L.  Coplin  for  permission  to  photograph  numer- 
ous specimens  in  the  Museum  of  Pathology  of  the  Jefferson  Medical 
College,  as  well  as  to  Dr.  David  R.  Bowen  and  to  Dr.  Henry  K.  Pancoast 
for  our  radiograms. 

The  Authors. 
Philadelphia,  Penna., 
July,  1917. 


1  The  photographs,  both  clinical  and  anatomical,  were  with  negligible  exceptions, 
made  by  Dr.  George  W.  Norris.  Many  of  the  pictures  illustrating  diseases  of  the 
heart  and  aorta  have  been  reproduced  from  "Studies  in  Cardiac  Pathology"  by 
George  W.  Norris. 

2 Geigel,  Richard:  "Leitfaeden  der  Diagnostischen  Akustik."     Stuttgart,  1908. 

3  Montgomery  and  Eckhardt:  "Pulmonary  Acoustic  Phenomena."  Tenth 
Annual  Report  of  the  Henry  Phipps  Institute,  Phila.,  1915. 

9 


CONTENTS 


PART  I 
THE  EXAMINATION  OF   THE  LUNGS 

By  George  W.  Norris,  A.  B.,   M.  D. 
CHAPTER  I 

Page 

Physical  Diagnosis 17 

Inspection,  17;  General  inspection,  19;  Inspection  of  the  chest,  20;  Abnormal 
thoracic  conformation,  32;  Abnormal  respiration,  39;  Visible  changes  in 
respiratory  rhythm,  41. 

CHAPTER  II 

Palpation 42 

Object  of  palpation,  42;  Cutaneous  hyperesthesia,  43;  Pleural  pain  or  hyper- 
esthesia, 44;  Tactile  or  vocal  fremitus,  45. 

CHAPTER  III 

Acoustics  in  Physical  Diagnosis 53 

Rhythmic  vibrations,  53;  Unrhythmic  vibrations,  54;  Vibrations  in  tense 
membranes,  54;  Sympathetic  vibrations,  54;  Interference  waves,  55;  Loaded 
strings,  55;  Resonators,  56;  Qualities  of  sound,  57;  Origin  of  sounds  heard 
over  chest,  59. 

CHAPTER  IV 

The  History  and  Theory  of  Percussion 63 

Percussion  sounds,  63;  Tympany,  63;  Resonance,  65;  Dulness,  66;  Hyper- 
resonance,  67;  Impaired  resonance.  68;  Flatness,  68;  Modified  tympany  68; 
Metallic  ring,  69;  Bell  tympany,  69;  Cracked-pot  sound,  69;  Special  per- 
cussion signs,  72. 

CHAPTER  V 

Anatomic  Considerations 73 

CHAPTER  VI 

Methods  and  Results  of  Percussion 79 

Immediate  or  direct  percussion,  79;  Mediate  or  indirect  percussion,  79; 
Results  of  percussion,  81;  Purpose  of  percussion,  86;  Technic  of  percussion, 
88;  Special  varieties  of  percussion,  88;  Conditions  modifying  percussion 
sounds,  90. 

11 


12  CONTENTS 

CHAPTER  VII 

Page 

Normal  Variations  of  Pulmonary  Percussion  Sounds 94 

Individual  variations,  94;  Regional  variations,  94;  Other  variations,  101; 
Diaphragm,  101;  Some  physiologic  considerations,  102. 

CHAPTER  VIII 

Auscultation      104 

Methods  of  auscultation,   104;  Influence  of  posture  on  physical  signs,  106; 
Stethoscopes,  107;  Breath  sounds,  109. 

CHAPTER  IX 

XORMAL  AND  ABNORMAL  BREATH  SOUNDS 113 

Normal  vesicular  sound,   113;  Abnormal  breath  sounds,   113;  Changes  in 
respiratory  rhythm,  121. 

CHAPTER  X 

Adventitious  Breath  Sounds 122 

Rales,  122;  Friction  sounds,  125;  Succussion  splash,  128;  Metallic  tinkle,  129. 

CHAPTER  XI 

Voice  Sounds : 130 

Vocal  resonance,   130;  Bronchophony,   132;  Pectoriloquy,   132;  Egophony, 
135. 

CHAPTER  XII 

Physical  Findings  in  Infants  and  Young  Children 136 

Chest  inspection,   136;  Palpation,  136;  Percussion.  136;  Auscultation,   139; 
Pathologic  conditions,  141;  Practical  considerations,  144;  The  X-ray,  147. 


PART  I 

THE  EXAMINATION  OF  THE  CIRCULATORY  SYSTEM 

By  George  W.  Xorris,  A.  B.,  M.  D. 

CHAPTER  XIII 

The  Circulatory  System 149 

Inspection,  149;  The  heart — Anatomic  considerations,  151;  Palpation  of  the 
pulse,  155;  Pulse  rhythm,  156;  Pulse  volume,  156;  Pulse  tension,  156;  Equal- 
ity of  the  pulse,  157;  Normal  and  abnormal  types  of  arterial  pulse,  157. 


CONTENTS  13 

CHAPTER  XIV 

Page 

Instrumental  Methods 161 

Blood-pressure  estimation,  161;  Venous  blood  pressure,  164;  Venous  pulse, 
164;  Sphygmographs,  165;  Interpretation  of  sphygmogram,  167. 

CHAPTER  XV 

Cardiac  Arrhythmia 168 

Normal  rhythm,  168;  Sinus  arrhythmia,  169;  Heart  block,  169;  Extrasystole, 
171;  Paroxysmal  tachycardia,  172;  Auricular  nutter,  173;  Auricular  fibrilla- 
tion, 173;  Pulsus  alternans,  175;  Soldier's  heart,  177;  Estimation  of  vaso- 
motor efficiency,  177. 

CHAPTER  XVI 

The  Electrocardiograph  (By  Dr.  Edward  B.  Krtjmbhaar) 179 

The  principle,  179;  Normal  electrocardiogram,  180;  Preponderating  ven- 
tricular hypertrophy,  182;  Cardiac  arrhythmias,  184. 

CHAPTER  XVII 

Palpation 193 

Cardiac  impulse,  193;  Thrills,  198. 

CHAPTER  XVIII 

Percussion  op  the  Heart 200 

Methods  and  technic,  200;  Significance  of  cardiac  dulness,  204;  Records  of 
cardiac  dimensions,  207;  Orthodiagraph,  208. 

CHAPTER  -XIX 

Auscultation 210 

Object  and  method  of  auscultation,  210;  Origin  and  character  of  heart 
sounds,  210;  Acoustics  of  heart  sounds,  212;  Individual  variation  of  the  heart 
sounds,  214;  Disproportionate  intensity  of  heart  sounds,  215;  Changes  in 
pitch  of  heart  sounds,  217;  Reduplication  of  heart  sounds,  217;  Changes  in 
rhythm  of  heart  sounds,  218. 

CHAPTER  XX 

Heart  Murmurs 220 

Acoustics,  220;  Technic  of  cardiac  auscultation,  222;  Variations  in  intensity 
of  heart  sounds,  222;  Endocardial  murmurs,  223;  Individual  valvular  mur- 
murs, 226;  Functional  murmurs,  240;  Effect  of  respiration  on  endocardial 
murmurs,  242;  Special  murmurs,  243;  Exocardial  murmurs,  246;  Venous 
murmurs,  247;  Cardio-respiratory  murmurs,  247;  Pericardial  friction 
sounds,  249. 


14  CONTENTS 


PART  III 

DISEASES  OF  THE  BRONCHI,  LUNGS,  PLEURA, 
AND  DIAPHRAGM 

By  H.  R.  M.  Landis,  A.  B.,  M.  D. 

CHAPTER  XXI 

Page 

Diseases  of  the  Bronchi 257 

Acute  bronchitis,  257;  Chronic  bronchitis,  259;  Fibrinous  bronchitis,  261; 
Bronchiolitis  fibrosa  obliterans,  265;  Whooping  cough,  267;  Bronchial 
asthma,  270;  Bronchiectasis,  276;  Fetid  or  putrid  bronchitis,  285;  Bron- 
chiolectasis,  286;  Foreign  bodies  in  the  air  passages,  287. 

CHAPTER  XXII 

Diseases  op  the  Lungs 293 

Tuberculosis  of  the  lungs,  293;  Chronic  tuberculosis  of  the  lungs,  293;  Acute 
tuberculosis  of  the  lungs,  361;  Fibroid  phthisis,  367;  Acute  miliary  tuber- 
culosis, 368;  Mycotic  infections  of  lungs,  378;  Streptothricosis,  378;  Actino- 
mycosis, 381;  Blastomycosis,  384;  Coccidioidal  granuloma,  387;  Aspergil- 
losis, 380;  Sporotrichosis,  390;  Acute  lobar  pneumonia,  391;  Friedlander's 
bacillus  pneumonia,  414;  Psittacosis,  416;  Broncho-pneumonia,  417;  Pulmon- 
ary fibrosis,  427;  Pneumoconiosis,  434;  Atelectasis,  445;  Emphysema,  449; 
Chronic  hypertrophic  emphysema,  449;  Senile  emphysema,  454;  Acute  ves- 
icular emphysema,  455;  Interstitial  emphysema,  455;  Compensatory 
emphysema,  456;  Pulmonary  abscess,  458;  Pulmonary  gangrene,  466;  Pul- 
monary infarction,  470;  Pulmonary  congestion,  475;  Pulmonary  edema, 
477;  Effects  of  poisonous  gases  on  the  respiratory  tract,  480;  Hydatid  dis- 
ease of  the  lungs  and  pleura,  484;  Pulmonary  distomatosis,  487;  Syphilis 
of  the  respiratory  tract,  490;  Intrathoracic  tumors,  498;  Enlargement  of 
the  thymus,  512;  Hernia  of  the  lung,  517;  Alterations  in  the  extremities 
due  to  chronic  pulmonary  disease,  518;  Changes  in  the  finger  nails,  518; 
Clubbing  of  the  fingers  and  toes,  519;  Hypertrophic  pulmonary  osteo-ar- 
thropathy,  522. 

CHAPTER  XXIII 

Diseases  of  the  Pleura 527 

Pleurisy,  527;  Dry  pleurisy,  533;  Fibrinous  pleurisy,  534;  Diaphragmatic 
pleurisy,  535;  Serofibrinous  pleurisy  (Pleural  effusion),  535;  Chronic  pleurisy, 
544;  Empyema,  544;  Encysted  empyema,  551;  Hemorrhagic  pleural  effusions, 
557;  Hemothorax,  559;  Chylothorax,  562;  Hydrothorax,  564;  Pneumothorax, 
568. 

CHAPTER  XXIV 

Diseases  of  the  Diaphragm 579 

Anatomy;  Normal  and  pathological  physiology  of  the  diaphragm,  579; 
Functional  disturbances  of  the  diaphragm,  582;  Diaphragmatic  hernia,  585; 
Evisceration  (Traumatic  or  spurious  hernia),  585;  Eventration  of  the  dia- 
phragm, 588;  Diaphragmatis,  591;  Subdiaphragmatic  abscess,  596. 


CONTENTS  15 

PART  IV 
DISEASES  OF  THE  PERICARDIUM,  HEART,  AND  AORTA 
By  H.  R.  M.  Landis,  A.  B.,  M.  D. 
CHAPTER  XXV 

Page 

Diseases  of  the  Pericardium 603 

Acute  fibrinous  pericarditis,  603;  Tuberculous  pericarditis,  606;  Pericardial 
effusion,  607;  Chronic  adhesive  pericarditis,  610. 

CHAPTER  XXVI 

Diseases  op  the  Myocardium 617 

Hypertrophy,  617;  Dilatation,  624;  Myocarditis,  626;  Aneurism  of  heart, 
633;  Myocardial  changes  due  to  syphilis,  636. 

CHAPTER  XXVII 

Endocarditis 640 

Acute  endocarditis,  640;  Malignant  endocarditis,  644;  Chronic  infectious 
endocarditis,  651;  Chronic  valvular  disease,  654;  Mitral  insufficiency,  661; 
Mitral  stenosis,  667;  Aortic  insufficiency,  676;  Aortic  stenosis,  681;  Tri- 
cuspid insufficiency,  685;  Tricuspid  stenosis,  689;  Pulmonary  insufficiency, 
693;  Pulmonary  stenosis,  695 

CHAPTER  XXVIII 

Congenital  Heart  Disease 698 

CHAPTER  XXIX 

Angina  Pectoris -.    . -.    .   708 

Angina  pectoris  major,  708;  Incipient  angina  pectoris,  712;  Angina  pectoris 
vasomotoria  (pseudo-angina),  713. 

CHAPTER  XXX 

Aortitis 716 

Acute  aortitis,  716;  Syphilitic  aortitis,  718;  Chronic  aortitis,  721. 

CHAPTER  XXXI 

Aneurism  of  the  Thoracic  Aorta 731 

Dilatation  of  the  aorta,  752;  Arterio-venous  aneurism,  756;  Aneurism  of 
innominate  artery,  756;  Rupture  of  the  aorta,  757. 

Index 761 


PART    I 
THE   EXAMINATION  OF  THE  LUNGS 

By  George  W.  Norris,  A.  B.,  M.  D. 


CHAPTER  I 

PHYSICAL  DIAGNOSIS 

Physical  diagnosis  consists  in  employing  our  senses — sight,  touch,  and 
hearing — to  determine  the  condition  of  the  tissues.  These  are  altered  in 
character  by  many  pathologic  states.  They  may  become  more  solid  or 
less,  may  contain  more  or  less  of  fluid  or  of  air  than  normal,  their  elas- 
ticity may  be  increased  or  diminished.  Again,  it  may  be  that  organs  be- 
come larger  or  smaller  than  normal,  or  are  shifted  more  or  less  out  of 
place.  Such  alterations  we  can  often  demonstrate  by  means  of  physical 
signs.  The  data  thus  obtained,  used  in  conjunction  with  a  knowledge  of 
the  patient's  history,  and  symptoms,  together  with  a  familiarity  with  the 
pathology,  often  permit  us  to  estimate  very  accurately  the  nature,  charac- 
ter, location  and  extent  of  the  disease  from  which  the  patient  is  suffering. 
"  The  significance  of  morbid  signs  relates  immediately  not  to  diseases,  but 
to  the  physical  conditions  incident  thereto.  Signs  are  not  directly  diag- 
nostic of  particular  diseases  "  (Flint) .  The  methods  employed  in  physical 
diagnosis  are:  inspection,  palpation,  percussion,  and  auscultation.  These 
methods  are  frequently  combined  with  mechanical,  chemical,  electrical, 
microscopic  and  bacteriologic  examination,  as  well  as  with  the  data 
obtained  by  means  of  the  X-rays. 

INSPECTION 

Although  seemingly  the  most  obvious,  the  simplest  and  the  easiest  of 
the  four  methods  mentioned,  accurate,  useful  and  skilled  inspection  is 
in  reality  often  the  most  difficult  to  acquire  and  the  last  in  which  the 
practitioner  becomes  proficient.  It  is  in  this  method  especially  that 
the  seasoned  physician  far  excels  his  younger  confrere.  This  is  in  part 
due  to  carelessness  on  the  part  of  the  younger  man,  but  is  perhaps  even 
more  due  to  the  fact  that  the  senior  has  become  accustomed  to  make 
note  of  many  items  at  a  glance,  and  also  that  he  has  learned  not  only 
what  to  look  for,  but  where  to  look  for  it,  and  how  to  read  the  facts 
which  are  presented  before  his  eyes.  He  has  acquired  the  faculty  of 
seeing  with  the  mind  as  well  as  with  the  eye.  "We  can  only  see  what 
we  have  learned  to  see."  Corrigan's  remark  is  still  as  apt  as  the  day  it 
was  uttered:  "The  trouble  with  most  doctors  isn't  so  much  that  they 
don't  know  enough,  as  it  is  that  they  don't  see  enough!"  We  feel 
2  17 


18 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.  1. — Clubbing  of  the  fingers  due  to  congenital  heart  disease. 


Fig.  2. — Radiogram  of  the  fingers  depicted  in  Fig.  1,  showing  not  only  hypertrophic 
changes  in  the  soft  tissues,  but  also  new  bone  formation  in  the  distal  phalanges  (pulmonary 
osteo-arthropathy).  "Simple  clubbing  of  the  fingers  and  secondary  hypertrophic  osteo- 
arthropathy should  be  considered  as  identical,  the  former  representing  an  early  stage  of  the 
latter."     {E.  A.  Locke.) 


INSPECTION  19 

that  we  cannot  over-emphasize  the  importance  of  careful,  intelligent 
inspection. 

The  Examination  of  the  Lungs. — For  the  purposes  of  examination, 
the  body,  especially  the  chest  and  abdomen,  must  be  stripped.  The  light 
should  be  good.  Its  source,  as  to  whether  it  falls  directly,  obliquely  or 
vertically,  upon  the  patient,  must  often  be  varied.  Many  physiologic 
and  pathologic  conditions  can  be  seen  only  with  oblique  illumination. 
It  is  therefore  desirable  to  have  the  patient  first  face  the  window,  later 
turn  his  side  toward  it.  In  the  latter  position  most  of  the  shadows 
become  intensified. 

The  following  points  are  especially  to  be  noted : 

GENERAL  INSPECTION 

General  appearance,  posture,  gait,  facial  expression,  nutrition,  color. 

Absolute  symmetry  is  unknown.     As  a  general  rule  the  right  side 

of  the  body  is  better  developed  than  the  left.     The  right  chest  is  about 


Fig.   3. — Pulmonary  osteo-arthropathy  of  the  hands  and  forearms  in  a  case  of  sarcoma  of 

the  lung. 

\}/2  inches  larger  in  circumference  than  the  left.  The  spine  curves  to- 
ward the  right,  the  right  arm  is  longer  and  the  corresponding  shoulder 
is  often  narrower  and  lower.  There  are,  of  course,  well-marked  dif- 
ferences which  depend  upon:  (a)  Sex:  These  involve  the  bones,  the 
pelvis,  the  genitalia,  the  panniculus  adiposus,  etc.  (6)  Age:  In  the 
child,  the  ribs  are  more  horizontal,  the  heart  and  liver  larger,  the  lungs 


20  THE    EXAMINATION    OF    THE    LUNGS 

smaller,  the  thymus  is  present,  the  bones  are  more  cartilaginous  (see 
p.  136). 

The  Skin. — (a)  The  color  (pallor,  cyanosis,  jaundice,  pigmentation, 
mottling,  etc.);  (6)  the  character  (texture,  moisture,  edema,  eruptions, 
gloss,  subcutaneous  fat,  wasting,  distended  blood-vessels). 

The  Muscles. — Development,  wasting,  tremors,  symmetry. 

The  Face. — Intelligence,  expression,  symmetry,  spasm,  paralysis, 
edema,  myxedema. 

The  Hair. — Dryness,  sparsity,  distribution,  dyes,  parasites,  local 
discoloration. 

The  Eyes. — Prominence  of  the  eyeballs,  the  pupils  (size,  color  sym- 
metry, equality,  reaction  to  light,  etc.),  conjunctiva  (color,  ecchymosis, 
discharges),  cornea  (transparency,  arcus  senilis,  leucoma). 

The  Mouth. — Teeth,  gums,  tongue,  pharynx,  tonsils,  lips  (cyanosis, 
herpes,  ulcerations,  moisture,  deposits,  drooping,  rhagades). 

The  Ears. — Shape,  discharges,  tophi,  scars. 

The  Nose. — Discharges,  obstruction,  motion  of  the  nostrils  (dyspnea), 
dilated  venules. 

The  Neck. — Pulsations — arterial  and  venous,  swelling— adenitis, 
thyroidal  enlargement,  scars. 

The  Hands. — Cyanosis,  curved  or  ridged  nails,  clubbed  fingers, 
joints,  deposits  (tophi,  Heberden's  nodes),  shape,  symmetrv,  nutrition, 
capillary  pulse  (Figs.  1,  2,  3,  310,  311,  312). 

The  Abdomen. — Shape,  distention,  varicosities,  asymmetry,  pulsation, 
edema,  eruptions. 

The  Legs  and  Feet. — Edema,  clubbing  of  the  toes,  deformities,  vari- 
cosities, cyanosis,  scars,  pigmentation. 

INSPECTION  OF  THE  CHEST 

This  method  of  physical  examination  is  too  frequently  omitted,  or 
made  so  hastily  and  cursorily  that  little  or  no  information  is  obtained. 
Inspection,  properly  done,  yields  more  valuable  information  than  any 
other  procedure  at  our  disposal,  with  the  exception  of  auscultation;  and 
furthermore,  it  has  this  to  commend  it,  namely,  that  no  special  training- 
is  required,  and  the  beginner,  providing  he  is  taught  to  use  his  eyes  in- 
telligently, is  as  capable  of  seeing  defects  as  the  experienced  observer. 
This  is  in  marked  contrast  to  the  training  necessary  to  educate  the  ear 
to  differentiate  sounds,  particularly  those  produced  by  percussion,  the 
latter  method  often  requiring  years  of  practice.  Inspection,  on  the  other 
hand,  requires  no  special  technique;  the  only  requirement  is  that  one 
should  keep  in  mind  constantly  that  every  abnor?nality,  however  slight  it 
may  appear,  is  worthy  of  consideration. 

One  who  has  been  taught  to  make  a  proper  inspection  can,  in  many 
instances,  come  to  a  fairly  definite  conclusion  from  this  procedure  alone. 
Since  inspection  requires  no  special  training,  it  is  particularly  valuable  to 
the  student,  and  to  those  who  see  chest  cases  incidentally,  and  not 
constantly. 

In  order  that  inspection  should  yield  the  best  results,  it  is  absolutely 
essential  that  the  patient  be  stripped  to  the  waist.  "The  unpleasant- 
ness and  inconvenience  to  a  patient  of  undressing  for  this  purpose,  the 
time  occupied  in  so  doing,  the  trouble  it  gives,  and  a  sense  of  delicacy  in 


INSPECTION 


21 


females"  are  no  longer  to  be  considered  the  serious  obstacles  Laennec 
believed  them  to  be.  An  examination  of  a  chest  which  has  not  been 
entirely  exposed  is  in  the  vast  majority  of  instances  worse  than  no  ex- 
amination at  all.  In  regard  to  women  it  can  be  safely  asserted  that  no 
difficulty  will  be  encountered  if  the  importance  of  the  procedure  is  ex- 
plained and  they  are  not  unnecessarily  exposed.  For  some  years  we 
have  used  the  following  method.  A  piece  of  linen  or  fine  muslin  a  yard 
square  is  slit  from  one  corner  to  the  center  and  the  free  edges  hemmed 
(see  Figs.  4  and  5).  This  is  thrown  over  the  shoulders.  In  examining 
the  anterior  aspect  of  the  chest  the  cape  is  loosened  over  the  shoulders. 
When  the  area  below  the  breasts  is  examined  the  cape  still  affords  pro- 
tection.    In  examining  the  back  the  cape  may  be  pushed  up  exposing 


Figs.  4  and  5. — The  examining  cape  in  use. 


the  entire  back  as  no  objection  is  ever  offered  to  this.  As  the  capes  are 
inexpensive  a  number  can  be  kept  on  hand  and  a  fresh  one  used  for  each 
patient. 

It  must  be  borne  in  mind  that  a  patient  stripped  to  the  waist  should 
not  be  subjected  to  the  discomfort  of  a  cold  examining  room. 

The  next  requisite  is  that  the  patient  shall  be  so  placed  that  the  light 
falls  directly  on  the  parts  under  inspection.  In  comparing  the  two  sides 
of  the  chest,  the  illumination  must  not  come  from  one  side  as  errors  may 
occur  if  one-half  of  the  chest  is  less  well  lighted  than  the  other.  The  chest 
should  be  inspected  not  only  from  the  anterior  and  posterior  aspects  but 
also  in  profile;  the  latter  method  is  of  value  in  estimating  the  depth  of  the 
chest  and  also  in  determining  the  presence  or  absence  of  pulsation.  In 
addition  the  chest  should  be  inspected  from  above  downward.  This 
is  done  by  the  examiner  standing  behind  the  patient  and  looking  down 
over  the  shoulders. 

The  Posture  of  the  Patient. — As  to  the  posture  of  the  patient,  the 
sitting  position  is  the  one  of  choice.     The  patient  should  be  instructed  to 


22 


THE    EXAMINATION    OF   THE    LUNGS 


assume  a  natural  posture  and  not,  on  the  one  hand,  to  sit  too  rigidly,  or, 
on  the  other,  to  assume  a  slouching  position.  The  standing  position  may 
be  selected  if  the  examiner  prefers  it.  It  is  not  as  convenient  and  if  the 
examination  takes  much  time  is  tiring  both  for  the  patient  and  the 
examiner. 

Inspection  of  the  chest  in  patients  who  are  confined  to  bed  and  acutely 
ill  is  never  as  satisfactory  as  in  those  who  can  sit  or  stand  up.  Further- 
more, only  the  anterior  aspect  of  the  chest,  as  a  rule,  is  available  for  the 
method.  Another  difficulty  is  that  in  private  houses  the  light  frequently 
comes  from  one  side  only,  so  that  half  of  the  chest  is  in  a  shadow  which 
seriously  interferes  with  a  good  view.  In  very  ill  patients  this  method 
of  physical  examination,  in  common  with  the  other  procedures,  suffers 
from  a  lack  of  thoroughness  which  is  often  unavoidable.  If  the  exami- 
nation of  the  patient  in  the  recumbent  attitude  is  unavoidable,  care 


Fig.   6. — The  topography  of  the  chest  anteriorly.      For  purposes  of  description  the  chest  is 
divided  into  certain  regions  which  are  shown  in  this  and  in  the  following  figure. 


should  be  taken  to  see  that  the  body  rests  on  an  even  plane;  otherwise 
the  results  may  be  affected  very  materially  (see  p.  196). 

To  fix  a  standard  of  what  constitutes  a  normal  chest  which  shall 
serve  as  a  criterion  by  which  to  estimate  either  the  existence  of  or  the 
degree,  of  abnormal  variations,  is  not  possible.  Individuals  entirely 
free  from  thoracic  disease  present  the  greatest  variations  in  the  conforma- 
tion of  their  chests. 

The  Conformation  of  the  Normal  Chest. — Providing  that  the  chest 
does  not  present  some  one  of  the  recognized  deformities,  it  is  assumed 
to  be  normal  if  it  is  symmetrical,  not  only  generally  but  in  its  different 
parts.  The  shoulders  should  be  on  the  same  level  and  the  line  from  the 
neck  to  the  point  of  the  shoulder  slightly  convex.  In  men  the  clavicles 
are  usually  more  or  less  prominent  and  the  supraclavicular  spaces  a  little 
depressed.  In  women  the  clavicles  are  not  uncommonly  hidden  by 
adipose  tissue  and  there  are  no  depressions  above  the  clavicles.  Beneath 
the  clavicles  the  chest  wall  is  slightly  convex.     The  intercostal  spaces  are 


INSPECTION 


23 


slightly  below  the  surface  unless  the  individual  is  well  covered  with  fat. 
Owing  to  the  progressively  increasing  obliquity  of  the  ribs  from  behind 
forward  the  intercostal  interspaces  are  broader  in  front  than  behind. 
In  the  majority  of  individuals  a  projection  of  the  sternum  is  visible  at 
the  level  of  the  second  costal  caertilags.  This  projection  or  angle  is  of 
variable  degree  and  is  formed  by  the  articulation  of  the  upper  and  middle 
portions  of  the  sternum.  It  is  known  as  the  Angulus  Sterni  or  Angle  of 
Louis.  In  certain  thoracic  conditions,  particularly  emphysema,  the 
bulging  forward  of  the  upper  ribs  tends  to  accentuate  this  angle.  The 
lower  part  of  the  sternum  just  above  the  ensiform  cartilage  is  normal^ 
slightly  depressed. 

Viewed  from  behind  the  angles  of  the  scapula  should  be  on  the  same 
level  (corresponding  to  the  spine  of  the  eighth  dorsal  vertebra)  and  closely 
approximated  to  the  chest  wall. 


Fig.  7. — The  topography  of  the  chest  posteriorly. 

The  spine  should  be  straight  and  slightly  concave  from  above  down- 
ward. Slight  deviations  of  the  spine  are  not  uncommon,  however,  and 
may  or  may  not  be  an  indication  of  thoracic  disease.  They  are  frequently 
due  to  faulty  posture. 

The  points  especially  to  be  noted  in  inspecting  the  thorax  are:  the 
size  and  development,  the  contour  and  symmetry,  the  mobility  or  degree 
of  expansion,  the  type  of  breathing,  the  rate  of  respiration,  the  degree  of 
the  subcostal  angle,  local  bulging  or  pulsation,  and  the  prominence  of 
the  clavicles. 

The  Size  of  the  Chest. — -The  development  of  the  chest  depends  to  a 
considerable  degree  upon  the  general  health  and  activity  of  the  individual. 
Hence,  large,  deep,  well-muscled  thoraces  are  found  in  robust,  physically 
active  men.  Small  flat  chests  are  seen  as  the  result  of  early  disease  neces- 
sitating long  periods  spent  in  bed;  rachitis,  and  nasal  obstruction  (ade- 


24 


THE    EXAMINATION    OF    THE    LUNGS 


noids)  are  also  common  causes.  Lack  of  thoracic  development  or  chest 
deformity  in  early  life  is  chiefly  due  to  these  causes.  In  adult  life  abnor- 
malities generally  result  from  tuberculosis,  pleuritis  or  emphysema. 

The  Contour  and  Symmetry  of  the  Chest. — It  is  especially  important 
that  the  two  sides  of  the  chest  be  compared  with  each  other.  There  is  of 
course  no  absolute  normal  standard,  but  merely  a  variable  range  of  the 
normal.  Disease  of  the  chest  is  so  frequently  unilateral  that  by  choosing 
the  "better"  side  we  are  enabled  to  estimate  a  given  individual's  normal. 
Asymmetry  of  the  thorax  is  often  due  to  abnormal  curvature  of  the 
spine — scoliosis,  kyphosis,  lordosis — which,  when  present  to  a  marked 
degree,  often  renders  examination  by  auscultation  and  percussion  very 
difficult  (Figs.  17  and  26). 

At  birth  the  chest  is  cylindrical  (Fig.  19) ;  this  form  gradually  develops, 
beginning  at  the  second  year,  into  the  elliptic  shape  of  adult  life  (Fig.  20) , 


Fig.  8. — Position  of  the  bony  thorax  during  inspiration  and  expiration.      {After  Barth.) 


to  revert  again  during  old  age  to  more  or  less  the  circular  contour  of 
childhood  (Figs.  25  and  33).  The  exact  contour  can  be  accurately  deter- 
mined by  means  of  the  cyrtometer — a  band  of  lead,  hinged  in  the  middle, 
which  is  firmly  applied  and  moulded  to  the  chest,  the  contour  of  which 
it  afterward  maintains. 

The  Mobility  of  the  Chest. — Chest  expansion,  the  difference  in  cir- 
cumference between  forced  inspiration  and  expiration  is  in  normal  men, 
about  2  inches.  Much  greater  degrees  of  mobility  are  found  in  indi- 
viduals accustomed  to  severe  physical  exercise.  Chest  expansion  can  be 
greatly  developed  during  adolescence  by  practice;  it  is  medically  of 
minor  importance  (Fig.  8). 

Inequality  of  expansion  has  great  significance.  The  main  point  to  be 
determined  is  whether  both  sides  of  the  chest  expand  equally.  The  most 
important  cause  of  unilateral  diminished  or  delayed  expansion  is  tuber- 
culosis of  the  lungs  or  pleura,  but  such  a  condition  also  results  from  one- 


INSPECTION 


25 


sided  pneumonia,  pleural  effusion  or  pleuritis  (pain),  pneumothorax,  etc. 
The  last  two  conditions  may  also  alter  the  shape  of  the  intercostal  space. 
In  chronic  cases,  inequality  is  generally  due  to  local  adhesions  and  con- 
tractions of  the  subjacent  tissues.  Unequal  expansion  may  rarely  be 
due  to  rachitis,  hemiplegia,  and  muscular  atrophy.  Diminution  or  delay 
of  apical  expansion  can  be  best  detected  by  standing  behind  the  seated 
patient  and  looking  downward  over  his  shoulders. 


Atd0rU>r      9Um 


FIG-   9, — Cross   section   of   the  right  lung  showing  the  direction  of  expansion.      {Keith.) 

(See  p.  52.) 


Apex 


Fig.   10. — Right   lung   from   the  side  showing   the   direction   of   expansion.      (Keith.) 

The  spirometer  is  an  instrument  for  gauging  the  capacity  of  the  lung 
by  noting  the  amount  of  air  the  patient  can  blow  into  it.  In  normal 
individuals  the  measure  of  lung  capacity  varies  directly  with  muscular 
development,  provided  that  the  patient  breathes  properly,  but  erroneous 
conclusions  may  be  drawn  from  spirometer  readings  unless  special  atten- 
tion be  given  to  the  method  of  breathing.     Capacities  of  190  c.c.  (9  cubic 


26  THE    EXAMINATION    OF   THE    LUNGS 

inches)  and  possibly  less  are  consistent  with  normal  lungs.  Low  values 
obtained  by  either  the  spirometer  or  by  the  degree  of  chest  expansion 
merely  indicate  poor  development  or  improper  breathing.  In  suspected 
pulmonary  disease  very  little  if  any  additional  aid  in  diagnosis  can  be 
thus  obtained. 


Fig.   11. — Vertical  section  of  the  right  lung  showing  the  direction  of  expansion.      (Keith.) 

The  Type  of  Breathing. — In  men  respiration  is  mainly  diaphragmatic, 
in  women,  costal. 

"By  study  of  the  living  thorax" in  health  and  disease  we  learn— That  the  dia- 
phragm is  the  great  means  of  inspiration :  That,  in  quiet  breathing,  the  chief  use  of 
the  intercostal  muscles  is  to  maintain  the  position  of  the  ribs  (or  the  expansion  of  the 
chest)  during  the  descent  of  the  diaphragm :  That,  when  the  descent  of  the  diaphragm 
is  hindered,  or  when  inspiration  becomes  more  laboured  than  natural,  the  intercostals 
contract  more  strongly,  so  as  to  dilate  the  chest  by  raising  the  ribs:  That,  when  in- 
spiration becomes  as  forcible  as  possible,  other  muscles,  which  act  by  raising  the  collar 
bones  and  first  ribs,  come  into  play,  namely,  the  sternomastoids,  scaleni,  omohyoids, 
and  upper  part  of  the  trapezii:  That  quiet  expiration  is  due  to  the  cessation  of  ali 
muscular  contraction :  That  forced  expiration  is  performed  by  means  of  the  abdom- 
inal muscles  (especially  the  recti),  the  latissimi  dorsi,  and  lower  part  of  the  trapezii. 
Add  these  corollaries :  That  the  diaphragm  and  intercostals  are  antagonist,  although 
they  concur  to  produce  one  and  the  same  result:  That  forced  inspiration  tells  upon 
the  upper  chest  and  true  ribs :  That  forced  expiration  tells  upon  the  lower  chest  and 
false  ribs"  (Gee). 

"Whether  respiration  be  mainly  costal  or  mainly  abdominal  depends 
on  the  relative  part  taken  in  the  act  by  the  ribs  and  the  diaphragm." 
The  better  developed  the  abdominal  muscles  are,  the  more  easily  can  the 
diaphragm  elevate  the  ribs,  and  the  more  "thoracive"  the  type  of  respi- 
ration. It  also  depends  on  "the  order  in  which  different  parts  of  the 
body  wall  come  into  action.  If  the  wave  begins  in  the  abdomen  and 
passes  upward,  the  type  is  abdominal;  if  it  begins  above  and  passes 
down,  the  type  is  costal"  (Hutchison). 

The  types  of  breathing  are  often  modified  by  disease ;  thus  the  pain  of 
an  acute  pleuritis  diminishes  expansion  especially  on  the  affected  side. 
Peritoneal  pain  diminishes  downward  movement  of  the  diaphragm  and 
produces  relatively  more  costal  breathing. 


INSPECTION 


27 


The  Rate  of  Respiration. — The  rate  of  respiration  in  adult  man  is 
from  16  to  20  per  minute.  In  healthy  adults  breathing  is  rhythmic  as 
long  as  they  are  unconscious  of  it.  In  infants,  in  whom  the  function  is 
imperfectly  established,  it  is  often  irregular.  To  insure  accuracy  the 
patient  should  never  know  that  we  are  observing  the  manner  and  the 
rate  of  his  breathing.  The  respiration  and  the  pulse  normally  bear  the 
relation  of  about  1  to  4. 


Fig.   12. 


-Radiogram  showing  the  position  of  the  diaphragm  during  expiration  and  in- 
spiration.    Note  the  effect  upon  the  position  and  shape  of  the  heart. 


A  constantly  increased  rate  of  respiration  generally  indicates  disease 
of  the  heart  or  lungs,  but  disease  of  the  peritoneum  and  hysteria  may  also 
cause  rapidity.  A  decreased  respiratory  rate  occurs  in  sleep  (25  per  cent, 
slower),  in  obstruction  to  the  air  passages  and  in  opium  poisoning. 

Normal  Ratio  between  Age,   Pulse,   Inspiration  and  Temperature 


Birth  to  2 

2  to  5 

years 

years 

122 

114 

30 

26 

43 

35 

141 

135 

50 

44 

149 

161 

5  to  9 

years 


9  to  12 
years 


Adult 


Pulse  rate 

Respiratory  rate.     T.  98° 

T    10'?°  f  Respiratory 
\  Pulse 
Respiratory 


T.  105c 


I  Pulse 


103 

89 

76 

25 

24 

17 

30 

29 

27 

128 

117 

106 

37 

31 

34 

136 

136 

136 

The  Subcostal  Angle. — By  this  is  meant  the  angle  at  which  the  ribs 
meet  at  the  ensiform  cartilage.  It  is  important  in  classifying  the  type 
of  chest  with  which  we  have  to  deal.  It  is  narrow  or  acute  in  the  long, 
flat  chest;  and  broad  or  obtuse  in  the  cylindrical  or  barrel-shaped  thorax 
(Fig.  13). 

Local  Bulging  or  Pulsation. — Local  prominence  of  the  chest  is  often 
due  to  rachitis  in  childhood  and  to  spinal  curvature.     The  precordium 


28 


THE    EXAMINATION    OF    THE    LUNGS 


(that  part  of  the  chest  which  overlies  the  heart)  is  often  normally  promi- 
nent, although  much  greater  degrees  of  bulging  are  seen  when  the  heart 
is  hypertrophied  (Fig.  15),  especially  in  children.  The  most  important 
pathologic  prominence  is  that  seen  at  the  base  of  the  heart  in  aneurism 
of  the  aorta  (Fig.  16).  Occasionally  disease  of  the  ribs  and  empyema 
cause  local  swelling.  In  emaciated  subjects  pulsation  of  the  subclavian 
arteries  may  be  visible.  Rhythmicity  practically  indicates  that  a 
pulsation  is  directly  connected  with  the  circulatory  apparatus.  Pulsat- 
ing empyemata  are  very  rare. 


Fig.    13. — Illustrating  the  angle  of  the  ribs  in  the  barrel-shaped  and  in  the  long,  flat  chest. 

{Fowler  and  Godlee.) 


.  Prominence  of  the  Clavicles, — This  depends  largely  upon  the  shape 
of  the  chest.  It  is  marked  in  thoraces  conforming  to  the  "long,  flat" 
type  and  hence  is  common  in  enteroptotic  individuals.  It  is  often  seen 
in  tuberculosis  of  the  pulmonary  apices,  and  when  unilateral  may  be 
regarded  as  an  index  of  the  degree  to  which  the  subjacent  tissues  have 
sunken  in  or  have  been  retracted  (Fig.  30). 

The  Diaphragmatic  Shadow. — {Phrenic  wave,  Litten's  'phenomenon) 
(Fig.  18). — If  a  moderately  thini person,  lying  on  a  bed  with  the  chest  ex- 
posed and  with  the  feet  pointing  directly  toward  the  window,  takes  slow, 
deep,  "abdominal"  inspirations,  a  shadow  will  be  seen  to  move  down  the 
lateral  aspect  of  the  chest  wall,  between  the  sixth  and  the  ninth  ribs. 
This  shadow  is  caused  by  the  fact  that  during  inspiration  the  diaphragm 
"peels  off"  from  the  inner  chest  wall  and  by  means  of  the  negative  pres- 
sure thus  produced,  causes  the  soft  tissues  to  fall  inward.  These  altera- 
tions of  pressure  correspond  with  in-  and  expiration  and  create  the  im- 
pression of  a  shadow  moving  down  the  chest  wall.  By  the  mobility  of 
the  shadow  and  by  the  extent  of  its  excursion,  we  are  enabled  to  deter- 
mine the  degree  of  diaphragmatic  motion  and  its  equality  on  the  two 
sides  of  the  body  (Fig.  18). 

Local  adhesions,  a  pneumonia,  or  a  pleural  effusion  would  diminish 
or  inhibit  the  shadow.     A  subdiaphragmatic  abscess    would,    on    the 


INSPECTION 


29 


Fig.  14. — Bulging  of  the  left  lower  chest,  which  pulsated  synchronously  with  the  heart 
even  after  aspiration  of  the  pleura,  due  to  an  aneurism  of  the  left  ventricle.  The  dotted 
area  represents  approximately  the  degree  of  pulsating  excursion.  (Patient  of  Dr.  J.  N. 
Henry.) 


Fig.  15. — Bulging  of  the  precordium  due  to  an  hypertrophied  heart  (mitral  obstruction) 
in  a  boy  of  14  years.  Note  the  poor  nutrition  and  underdevelopment  often  caused  by 
cardiac  lesions  in  childhood. 


30 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.   16. — Deformity  of  the  chest  due  to  thoracic  aneurism. 


Fig.   17.— Deformity  of  the  chest  resulting  from  kypho-scoliosis.     Abnormal  physical  signs 
must  be  construed  with  great  caution  in  these  cases.     (See  Figs.  26,  83,  84.) 


INSPECTION 


31 


Fig.  IS. — Diaphragm  phenomenon  (Litten's  sign),  from  a  patient  with  fibroid  phthisis 
of  left  lung  (New  York  City  Hospital).  The  linear  shadow  has  been  emphasized  in  the 
reproduction  of  the  photographs.  .  , 

1.  Full  Expiration. — Note  the  height  of  the  shadow  and  the  slight  concavity  ot  the 
abdomen  corresponding  to  the  respiratory  phase. 

2.  Medium  Inspiration. — Note  the  descent  of  the  linear  shadow  and  the  slight  change  ot 
contour  of  abdomen  corresponding  to  the  respiratory  phase.  , 

3.  Deep  Inspiration. — Note  the  further  descent  of  the  linear  shadow  and  the  rigid 
abdomen  corresponding  to  the  respiratory  phase.  . 

Although  the  artist  has  intensified  the  shadow  in  the  reproduction,  the  excursion  ol  the 
right  lung  and  right  side  of  the  diaphragm  were  so  pronounced  m  this  patient  that  the  dis- 
tance between  the  shadows  in  the  extreme  positions  of  respiration  was  greater  than  has  been 
represented.  The  patient's  left  lung  was  practically  useless;  hence  the  abnormal  extent  ot 
the  right  lung's  excursion.     (Sahli  and  Potter.) 


32 


THE    EXAMINATION    OF   THE    LUNGS 


other  hand,  have  per  se  no  effect  on  the  excursion.  The  shadow  is  seen 
with  difficulty  in  (1)  obese  subjects,  (2)  if  there  is  more  than  one 
source  of  light,  (3)  if  costal  breathing  is  practised.  The  extent  of 
the  normal  excursion  ranges  between  2}4  and  3}^  inches,  depending 
upon  the  depth  of  respiration.  The  observer  may  stand  between  window 
and  patient,  or  may  have  the  patient  between  himself  and  the  window. 
Diaphragmatic  mobility  can,  of  course,  be  much  more  accurately 
determined  by  means  of  the  fluoroscope  but  in  the  absence  of  such  an 
apparatus  the  shadow  test  may  be  of  considerable  diagnostic  utility. 
Unilateral  immobility  or  diminished  diaphragmatic  excursion  generally 
results  from  pleurisy.  Among  83  cases  studied  by  Pryor  53  showed  com- 
plete immobility,  and  17  some  restriction  of  motion,  in  patients  who  had 
previously  had  pleural  effusions. 

ABNORMAL  THORACIC  CONFORMATION 

As  a  result  of  disease,  the  shape  of  the  chest  often  becomes  altered 
from  the  average  normal  type.  There  are,  of  course,  also  congenital 
tendencies  which  have  their  influence,  but  practically  the  shape  of  the 
chest  is  due  to  postnatal  influences.     Freund  and  others  maintain  that 


Fig.  19. — Transverse 
section  of  an  infant's  chest. 
Its  shape  is  cylindrical. 


Fig.  20. 


-An   adult's  chest,  elliptical   in 
shape. 


thoracic  development  is  absolutely  determined  as  regards  its  ultimate 
form  by  the  rapidity  of  growth  and  time  of  calcification  of  the  first  rib. 

The  length  of  the  normal  first  rib : 

Male  Female 

According  to  Freund  is 3.8  cm.     3 . 1     cm. 

According  to  Hart  is 3.6  cm.     3 .  02  cm. 

In  flat-chested  (phthisical)  individuals  it  measures  from  3  down  to  2.2  cm.  This 
makes  the  upper  chest  much  narrower  and  since  the  rib  is  also  more  sloping,  makes  the 
whole  antero-posterior  thoracic  diameter  small.  The  first  costo-sternal  articulation 
is  frequently  ossified.  Ih  thoraces  having  this  conformation  the  pulmonary  apices 
are  more  slender  and  respiratively  less  mobile.  It  is  to  these  factors  that  the  pre- 
disposition to  tuberculosis  is  supposed  to  be  in  part  due. 

Pathologic  deformities  of  the  chest  may  be  classified  among  the  fol- 
lowing types: 

I.  The  Rachitic  Chest. — The  rickety  (rachitic)  chest  (due  to  unduly  soft 
bones  during  its  development)  is  typically  characterized  by  (1)  beading 


INSPECTION 


33 


Fig.   21. — The    rachitic 
chest. 


Fig.  22. — The.  funnel-breasted  chest. 
(Compare  Fig.  30.) 


Fig.  23.— The  fiat  chest. 


Fig.    24. — Unilateral   retraction  of    the 
chest  due  to  pulmonary  fibrosis. 


Fig.  25. — The'emphysematous  chest. 
(Compare  Fig.  33.) 
3 


Fig.  26. — The  chest  in  scoliosis. 
(Compare  Fig.  17.) 


34 


THE    EXAMINATION    OF    THE    LUNGS 


of  the  costo-chondral  junctions  (rachitic  rosary),  (2)  a  transverse  fur- 
row corresponding  to  the  attachment  of  the  diaphragm  (Harrison's 
groove),  (3)  prominence  of  the  sternum  (pigeon  breast),  (4)  a  longitudinal 
groove  parallel  to  the  sternum  extending  to  the  costal  margin. 

During  infancy  respiration  is  mainly  abdominal,  because  the  thorax 
is  already  cylindrical  and  admits  of  but  little  further  outward  expansion. 
The  negative  intrathoracic  pressure  occasioned  by  the  descent  of  the 
diaphragm  exerts  its  effects  mainly  on  the  lower  ribs.  The  atmospheric 
pressure  causes  the  most  yielding  portion  of  the  thorax  to  cave  in  (costo- 
chondral  articulations)   and  thus   a  depressed  groove,   parallel  to  the 


Fig.  27.- 


-Normal  chest  with  excellent  conformation  and  muscular  development, 
pigmented  area  above  the  left  nipple  is  the  result  of  a  recent  blister. 


The 


sternum  is  formed.  Such  deformities  may  result  from  normal  breathing, 
but  are  much  enhanced  in  case  of  inspiratory  dyspnea.  Forced  inspira- 
tion, which  overexpands  the  upper  chest,  causes  a  forward  protrusion  of 
the  sternum  which  results  in  "pigeon  breast"  (Fig.  29).  This  may  be 
unequal  in  degree  on  the  two  sides  as  the  result  of  scoliosis.  The  chest 
is  usually  shortened,  and  the  costal  angle  acute.  Occasionally  there 
may  be  a  depression  of  the  sternum  extending  from  the  middle  of  the 
gladiolus  to  the  ensiform  cartilage  (funnel  breast,  trichter  brust,  pectus 
excavatum),  (Figs.  28  and  30).  Although  this  deformity  is  usually  con- 
genital, it  may  be   occupational  (schuster  brust,  cobbler's   breast)  due 


INSPECTION 


35 


Fig.  28. — A  rachitic  deformity  of  the 
chest  which  produced  a  very  pronounced 
dextrocardia. 


Fig.   29. — Pigeon   breast  in   a   cretinoid 
dwarf,  aged  23  years. 


Fig.  30. — Funnel  breast  due  to  rachitis, 
in  a  patient  who  ultimately  developed  pul- 
monary tuberculosis.  {Patient  of  Dr.  Ward 
Brinton.)      (Compare  Fig.  32.) 


Fig.  31. — Long,  flat  chest  with  marked 
retraction  and  emaciation,  in  a  case  of 
chronic  pulmonary  tuberculosis.  {Cour- 
tesy of  Dr.  Frescoln.) 


36 


THE    EXAMINATION    OF    THE    LUNGS 


to  external  pressure  from  tools  of  trade.     A  transverse  section  of  a  pigeon 
breast  is  triangular  in  form  (Fig.  22). 

II.  The  Long  Flat  Chest.— The  flat  (phthisinoicl,  paralytic)  chest  is 
commonly  met  with  in  pulmonary  tuberculosis,  and  while  apparently 
predisposing  to,  is  often  the  result  of,  this  disease.  It  is  a  chest  of  dimin- 
ished capacity  and  functionation.  The  thorax  is  elongated;  the  normal 
elliptical  shape  is  flattened  (antero-posterior  diameter  relatively  de- 
creased), the  subcostal  angle  is  acute,  and  the  obliquity  of  the  ribs 
increased.  In  association  we  often  see  faulty  posture  (stoop  shoulders, 
pot  bellies),  poor  expansion,  a  long  neck  with  a  prominent  larynx  and 
the  head  carried  forward.     Increased  obliquity  of  the  ribs  makes  the 


Fig.  32. — Plaster  cast  of  a  long  flat,  and  a  normal  chest.      (Houseman.) 


scapulae  prominent  (winged)  and  in  such  cases  we  speak  of  the  "ptery- 
goid" or  "alar"  chest,  especially  if  the  lateral  diameter  be  small.  The 
clavicles  are  prominent,  the  supra-  and  infraclavicular  fossae  exaggerated 
and  the  interspaces  wide.  Xot  infrequently  rachitic  deformities,  and 
especiallv  unilateral  deformities  due  to  pulmonarv  fibrosis  are  superadded 
(Figs.  30,  31,  and  32). 

III.  The  Barrel-shaped  Chest. — In  the  emphysematous  (barrel- 
shaped)  chest  the  normal  elliptical  form  tends  to  become  cylindrical  (the 
cylinder  has  a  greater  cubic  capacity).  The  ribs  are  elevated  and  everted 
(position  of  forced  inspiration) ;  as  a  result  of  this  the  costal  angle  en- 
larges, the  lower  ribs  flare  upward,  and  the  sternum  is  arched;  while 
Louis'  angle  becomes  prominent. 

These  changes  are  bilateral  and  result  from  enlarged  thoracic  con- 
tents— enlarged  lungs,  emphysema.  If  the  spine  is  also  involved  it 
becomes  bent  backward,  the  shoulders  are  thrown  forward  and  the  back 
is  rounded  (Fig.  34). 


INSPECTION 


37 


Fig.  33. — Barrel-shaped  chest,  a  case  of  long-standing  pulmonary  emphysema. 

(Compare  Fig.  25.) 


Fig.  34. — Emphysematous  chest  with  marked  kyphosis.     {Patient  of  Dr.   Ward  Brinton.) 


38  THE  EXAMINATION  OF  THE  LUNGS 

This  type  of  chest  is  the  result  of  prolonged  dyspnea — asthma, 
emphysema — owing  to  which  the  accessory  muscles  of  respiration  (sterno- 
mastoids,  serrati  postici  superiores,  serrati  antici  ma j ores,  trapezii, 
rhomboids,  levatores  scapulae,  and  the  pectoral  muscles)  hypertrophy. 
The  neck  becomes  thick  and  short,  the  thorax  being  drawn  upward. 
Inasmuch  as  the  expiratory  muscles  are  also  called  upon  for  increased 
effort  the  abdominal  muscles,  the  quadrati  lumbori,  and  serratus  anticus 
major  also  become  enlarged. 


Fig.  35. — Contrasted  Types.  The  young  man  on  the  left — a  case  of  advanced  pulmo- 
nary tuberculosis — has  a  long,  flat  chest.  The  ribs  are  obliquely  placed,  the  antero-posterior 
diameter  is  decreased,  expansion  is  almost  nil.  The  neck  is  long,  the  larynx,  clavicles  and 
scapula?  prominent. 

The  old  man  on  the  right- — a  case  of  pulmonary  emphysema — has  a  barrel  shaped  chest. 
The  ribs  are  horizontal,  the  spine  is  arched,  the  antero-posterior  diameter  is  increased,  the 
neck  is  short,  the  accessory  muscles  of  respiration  are  hypertrophied,  the  jugular  veins  are 
distended. 

In  some  cases  only  the  upper  part  of  the  chest  is  involved.  The 
emphysematous  chest  is  in  varying  degree  a  normal  senile  change,  it 
is  also  seen  in  individuals  whose  occupations  require  habitual  stooping, 
especially  if  associated  with  great  respiratory  demands — laborers,  sawyers. 
The  most  typical  examples  occur  in  sufferers  from  emphysema  especially 
if  associated  with  asthma.  The  supraclavicular  fossae  are  full  and  may 
actually  bulge  during  expiration  (see  Figs.  13,  25,  32,  33). 


INSPECTION  39 

Mixed  Deformities. — Various  combinations  of  the  foregoing  types 
may  sometimes  exist. 

There  may  also  be  unilateral  enlargement,  depression  or  bulging. 
Such  changes  are  usually  due  to  spinal  abnormalities,  or  to  pleural  and 
pulmonary  fibrosis. 


Fig.  36. — Chest  deformity  resulting  from  kypho-scoliosis.     (See  p.  92.) 
(Compare  Figs.  17,  26,  34.) 

ABNORMAL  RESPIRATION 

Dyspnea. — This  term  is  applied  to  various  types  of  "shortness  of 
breath."  It  generally  means  rapid,  labored  respiration  but  is  also  applied 
to  the  slow  difficult  breathing  which  occurs  when  the  larynx  or  the  trachea 
is  obstructed.  Dyspnea  may  occur  in  isolation,  during  either  phase  of 
respiration,  inspiration  or  expiration,  but  usually  both  acts  are  affected. 
It  is  due  to  either  (1)  lack  of  oxygen,  or  (2)  excess  of  carbon  dioxid  in  the 
blood.  As  a  general  rule  the  rate  and  the  depth  of  respiration  bear  an 
inverse  ratio  toward  each  other. 

Inspiratory  dyspnea  without  obstruction  simply  causes  increased 
thoracic  movement;  with  obstruction  it  causes  an  overexpansion  of  the 
upper  and  a  recession  of  the  lower  chest.  This  in  rachitic  children 
produces  marked  deformities. 

Expiratory  dyspnea  occurs  in  asthma,  emphysema  and  edema  of  the 
glottis.  Expiration  is  prolonged  and  laborious,  the  accessory  expiratory 
muscles  are  called  into  activity. 

Orthopnea  is  exaggerated  dyspnea,  in  which  the  patient  is  no  longer 
able  to  breathe  in  recumbency,  but  is  forced  to  sit  up  and  frequently  add 
the  additional  support  of  his  hands,  in  order  to  fix  the  muscles  of  the 
shoulder  girdle  and  thus  assist  the  accessory  muscles  of  respiration.  It 
is  characteristically  seen  when  the  lungs  are  congested  as  the  result 
of  tricuspid  insufficiency,  and  indicates  that  the  last  line  of  reserve  force 
has  been  called  into  action. 


40 


THE    EXAMINATION    OF    THE    LT/NGS 


Asthma  is  an  intermittent  form  of  dyspnea  in  which  expiration  is 
chiefly  affected.  The  latter  is  often  audible  at  a  distance  from  the  patient 
as  a  musical  wheezing  sound.  When  marked,  it  is  accompanied  by 
cyanosis,  a  sense  of  thoracic  constriction  and  of  suffocation.  It  is  due 
to  obstruction  of  the  bronchi,  either  spasmodic  or  edematous  in  nature, 
and  is  accompanied  by  the  expectoration  of  tenacious  glairy  mucus. 
Asthma  is  frequently  an  anaphylactic  manifestation. 

X  on-expansive  Dyspnea. — In  this  type  of  breathing  the  chest  is  ele- 
vated but  does  not  expand.  It  occurs  if  the  lung  is  impermeable  to  air 
(pneumothorax),  or  if  the  thorax  is  already  distended  to  the  limit  of  its 
capacity  (large  pleural  effusions,  extreme  emphysema)  or  if  expansion 
is  prevented  by  dense  pleural  adhesions  (pulmonary  fibrosis). 


Pig.  37. — An  example  of  the  adult  type  of  Cheyne-Stokes  breathing,  showing  the  large 
number  of  respirations  in  each  period,  the  relatively  short  apneic  pause  and  the  high  levels 
reached  by  the  expiratory  up-strokes  in  the  abdominal  trace.  In  this  and  the  following 
tracings  the  upper  line  represents  the  thoracic  tracing,  the  middle  line,  the  abdominal 
tracing,  and  the  bottom  line,  the  time  in  seconds.  The  down  strokes  record  the  inspiratory 
movements.      (Conner  and  Stilh?ian.) 

Restricted  or  " catchy"  respiration  may  occur  in  acute  pleuritis  or 
intercostal  neuritis  as  a  result  of  pain. 

Stridulous  breathing  is  characterized  by  a  noisy,  high-pitched,  crowing 
or  whistling  expiration.  It  is  due  to  a  spasmodic  condition  of  the  vocal 
cords  which  occurs  in  children. 

Stertorous  breathing  may  be  heard  at  a  distance  from  the  patient. 
It  occurs  in  comatose  and  moribund  patients,  and  consists  of  rattling, 
snoring  or  bubbling  sounds.  Its  genesis  is  akin  to  that  of  snoring,  since 
it  is  often  due  to  vibrations  set  up  by  the  soft  palate,  glottis,  tongue  or 
vocal  cords.  Not  infrequently,  however,  it  is  due  to  exudate  in  the 
trachea  or  large  bronchi,  which  is  thrown  into  vibration  by  the  act  of 
breathing,  as  for  instance  in  case  of  pulmonary  edema. 

The  death  rattle  is  a  combination  of  stertorous  breathing  combined 
with  the  rattling  caused  by  the  vibration  of  exudate  (serum,  pus,  blood) 
in  the  large  bronchi  and  the  trachea. 


INSPECTION 


41 


VISIBLE  CHANGES  IN  RESPIRATORY  RHYTHM 

Cheyne-Stokes  Respiration. — This  is  characterized  by  visible  irregu- 
larity of  breathing.  The  respirations,  shallow  at  first,  gradually  increase 
in  depth  and  rapidity,  to  be  followed  after  graduahV  diminishing  excur- 
sions by  complete  apnea,  lasting  sometimes  nearly  30  seconds  (Fig.  37). 
It  occurs  in  the  coma  of  uremia,  apoplexy,  meningitis,  opium  poisoning, 
etc.  Blood-pressure  is  higher  during  the  hyperpneic  periods,  in  cases 
associated  with  increased  intracranial  tension.  It  is  due  to  an  obtunded 
sensibility  of  the  medulla  to  C02.  Deep  breathing  carries  off  the  excess 
of  this  substance  and  the  respiratory  center  remains  inactive  until  another 


mAnprwY1^ 


tfMA/l/W 


yin/vyi  frrJ^\  /l/^rri^^^^^^^^iiL'r 


FlG.  3S. — Tracing  from  a  child  of  8  years,  showing  typical  Biot's  breathing.  Note  the 
pauses  which  occur  at  irregular  intervals  and  vary  in  length,  the  frequent  deep  sighs,  and 
the  constant  irregularity  of  the  respirations  in  force  and  rhythm.      (Conner  and  Stillman.) 


over-accumulation  of  this  gas  has  taken  place.  Cheyne-Stokes  respira- 
tion is  of  grave,  but  not  necessarily  fatal,  import.  In  children,  if  asso- 
ciated with  other  suggestive  symptoms,  it  points  gravely  toward  a 
meningitis. 

Biot's  Breathing. — This  type  of  breathing  differs  from  that  just 
described,  in  that  a  series  of  rapid  but  equally  deep  respiratory  movements 
is  followed  by  a  sudden  apnea.  There  is  no  gradual  increase  and  decrease 
in  the  depth  of  respirations  (Fig.  38).  'It  may  be  regarded  as  almost 
pathognomonic  of  meningitis  {Conner  and  Stillman1). 

1  Coxxer  and  Stillmax:  "A  Pneumographic  Study  of  Respiratory  Irregularities 
in  Meningitis."     Arch.  Int.  Med.,  ix,  1912,  203. 


CHAPTER  II 

PALPATION 

By  palpation  we  refer  to  the  use  of  the  sense  of  touch  for  the  determina- 
tion of  the  physical  character  of  the  tissues.     It  is  employed: 

1.  To  elicit  tenderness,  or  rigidity. 

2.  To  determine  the  presence  of  the  cardiac  impulse,  pulsations  or 
thrills,  and  to  feel  the  pulse  (see  Chap.  XIII). 

3.  To  determine  the  character  of  the  skin  (temperature,  moisture, 
texture,  edema). 

4.  To  discover  local  swelling,  induration,  softening,  etc.,  of  the  tissues, 
especially  as  regards  the  lymph  nodes. 


Fig.  39.  Fig.  40. 

Figs.  39  axd  40. — Palpation  to  determine  expansion  and  vocal  fremitus. 

.5.  To  estimate  the  degree  and  equality  of  chest  expansion. 

6.  To  elicit  vocal  fremitus. 

7.  To  determine  the  presence  of  hepatic  or  splenic  enlargement, 
pulsation  of  the  liver,  etc. 

Chest  Expansion. — The  bilateral  equality  of  chest  expansion  can 
often  be  satisfactorily  determined  by  laying  the  hands  lightly  upon  the 
patient's  chest  during  the  act  of  respiration.  Some  examiners  prefer  this 
method  to  simple  inspection. 

42 


PALPATION  43 

ZONES  OF  CUTANEOUS  HYPERESTHESIA  'HEAD'S  AREAS),  AND  REFLEX 

PAIN 

"  The  nerves  supplying  the  skin  and  skeletal  muscles  have  become  so 
educated  that  any  injury  to  them  is  accurately  located.  _  Such  is  not 
the  case  with  nerves  of  the  internal  organs.  A  painful  irritation  of  the 
viscera  finds  expression,  not  necessarily  over  the  site  of  the  organ,  but 
in  a  painful  area  of  the  skin  often  remote  from  it.  Head  has  shown  that 
the  painful  stimulus  in  the  organ  travels  in  a  centripetal  direction  to  the 
posterior  part  of  the  cord  and  there  sets  up  excitation  of  the  nerves  which 
in  the  same  and  in  the  adjoining  segments  supply  the  peripheral  surfaces 
with  sensation.  The  pain  is  referred  to  the  skin  because  therein  the  pain 
sense  reaches  its  highest  development."1 


Fig.  41. — Referred  pleural  pain.  The  horizontal  lines  indicate  the  location  of  inter- 
costal nerve  pain;  the  dots  represent  phrenic  nerve  pain,  on  the  anterior  surface  of  the 
body. 

"  Referred  pain  from  the  viscera  has  these  characteristics  to  differen- 
tiate it  from  pain  of  peripheral  origin:  (1)  It  is  often  remote  from  the 
site  of  irritation.  (2)  It  follows  the  lines  on  the  skin  of  the  spinal  seg- 
mentation rather  than  the  course  of  the  peripheral  nerves.  (3)  It  is 
usually  associated  with  cutaneous  hyperesthesia  and  tenderness  to  pres- 
sure. (4)  Often  the  pain  fails  to  involve  the  whole  segmental  area  of  the 
skin,  but  finds  expression  in  one  or  more  points  of  maximal  tenderness 
and  spontaneous  pain." 

Examples. — The  pain  of  biliary  colic  is  felt  at  the  angle  of  the  scapula, 
that  of  renal  colic  in  the  testicles,  while  heart  pain  is  referred  to  the  arm 
or  the  neck. 

Hyperesthesia  of  the  skin  is  determined  by  light  pressure  with  a  dull 
object  such  as  the  head  of  a  pin,  or  by  slight  pinching.     Muscular  rigidity 

^apps:  Arch.  Int.  Med.,  December,  1911. 


44 


THE    EXAMINATION    OF    THE    LUNGS 


or  spasm  which  may  have  a  similar  genesis  is  elicited  by  estimating  the 
degree  of  muscular  tonus  by  means  of  our  sense  of  touch. 


PLEURAL  PAIN 


The  parietal  pleura  and  outer  part  of  diaphragm  receive  their  nerve 
supply  from  the  lower  six  intercostal  nerves.  Lesions  in  this  region 
produce  pain  in  the  overlying  skin,  which  may  be  regarded  as  the  result 
of  a  peripheral  neuritis.     Cutaneous  hyperesthesia  is  absent.     Irritation 


Fig.  42. 


Fig.  43. 


Figs.  42  and  43. — Referred  cardiac  pain.  Showing  the  area  of  pain  and  cutaneous 
hyperesthesia  frequently  met  with  in  angina  pectoris.  The  segmental  distribution  (third 
cervical,  to  the  third  dorsal)  is  indicated  by  the  Roman  numerals.  Other  segments  may, 
however,  be  involved,  the  sixth  dorsal  causing  epigastric  pain,  and  the  upper  cervical  roots, 
pain  in  the  neck  and  back  of  the  head.  The  characteristic  sense  of  thoracic  constriction  has 
been  explained  as  resulting  from  reflex  stimulation  of  the  intercostal  muscles,  and  the  sense 
of  impending  dissolution  has  been  likened  to  the  violent  stimulation  of  the  nervous  system 
produced  by  excitation  or  injury  of  other  viscera,  as  by  a  blow  on  the  testicles  or  over  the 
solar  plexus.      (Mackenzie.) 

In  pulmonary  disease  cutaneous  hyperalgesia  occurred  in  3  per  cent,  of  the  460  cases  studied  by 
Langstroth  and  in  13  per  cent,  of  those  who  complained  of  pain.  In  disease  of  the  heart  and  aorta  the 
hyperalgesia  was  noted  in  7  per  cent.;  and  in  18  per  cent,  of  the  cases  having  pain.  As  a  diagnostic 
aid  the  occurrence  of  Head's  hyperalgesic  zones  is  generally  disappointing,  owing  to  the  large  number  of 
areas  over  which  disease  of  a  given  viscus  may  cause  sensory  changes. 


of  the  posterior  part  produces  pain  in  lower  chest,  abdomen  or  lumbar 
region.  This  is  a  referred  pain — by  way  of  the  seventh  to  the  twelfth 
dorsal  segments.  The  visceral  pleura  is  devoid  of  the  pain  sense.  The 
central  diaphragmatic  pleura  is  supplied  by  the  phrenic  nerve.  Irrita- 
tion of  this  region  produces  pain  and  tenderness  in  the  neck,  especially 
along  the  ridge  of  the  trapezius  muscle,  often  with  a  surrounding  zone 
of  hyperesthesia  (Fig.  41).     This  is  a  true  referred  pain — by  way  of  the 


PALPATION 


45 


third  and  fourth  spinal  segments.  The  pericardial  pleura  when  irritated 
may  produce  similar  pain,  because  its  nerve  supply  is  mainly  if  not  en- 
tirely phrenic  in  origin  (Capps). 

Pleural  pain  may  be  referred  to  the  abdominal  wall  and  lack  of  a 
careful  examination  of  the  lungs  has  led  to  unwarranted  celiotomies  in 
patients  who  a  day  or  two  later  have  developed  well-marked  signs 
of  the  pneumonia  which  was  the  cause  of  the  original  abdominal  pain 
and  rigidity.  Vice  versa,  although  less  frequently,  abdominal  lesions 
may  occasionally  produce  thoracic  pain. 


TACTILE  OR  VOCAL  FREMITUS 

Fremitus  is  the  tactile  perception  of  vibrations,  which  may  be  pro- 
duced by  (1)  phonation  (vocal  fremitus),  (2)  coughing  (tussive  fremitus), 
(3)  breathing  (rhoncal  fremitus)  produced  by  exudation  into  or  stenosis 
of  the  air  passages. 


Fig.  44. — Ulnar  palpation.  The  lower  pulmonary  border  can  be  accurately  determined 
by  laying  the  ulnar  surface  of  the  hand  and  little  finger  against  the  chest  wall  while  the 
patient  counts  one — one — one — .     (See  Fig.  50.) 

These  phenomena  set  up  vibrations  within  the  bronchi  and  lungs, 
which  under  favorable  conditions  are  accompanied  by  objectively  sensible 
vibrations  of  the  chest  wall,  which  can  be  felt  when  the  hand  is  laid 
upon  it,  as  a  faint  vibration  or  trembling  of  its  surface.  The  sensation 
thus  obtained  has  been  likened  to  that  derived  from  a  purring  cat,  but 
in  the  case  of  human  fremitus  the  vibrations  are  much  finer  and  more 
rapid. 

Vocal  fremitus,  which  only  is  of  practical  utility,  is  elicited  by  laying 
the  ulnar  surface  of  the  hand  or  fingers  upon  the  chest  or  in  the  inter- 


46 


THE    EXAMINATION    OF    THE    LUNGS 


costal  spaces,  while  the  patient  slowly  repeats  the  numerals,  "  one — one 
— one,"  or,  "ninety-nine"  in  a  clear,  low  tone.  Symmetric  areas  of  the 
chest  are  then  compared  in  regard  to  the  intensity  of  the  vibrations 
which  are  felt.  In  order  to  appreciate  the  mechanism  and  significance 
of  fremitus  we  must  revert  for  a  moment  to  that  of  voice  production. 

The  Mechanism  of  Voice  Production. — The  larynx  is  a  reed  instru- 
ment, the  pitch  of  which  is  determined  by  the  length  and  tension  of  the 


Fig.  45. — Diagram  illustrating  the  similarity  in  mechanism  between  voice  production 
in  the  human  body,  and  sound  production  in  an  organ.  From  above  downward  the 
angulated  lines  indicate  respectively:  A,  the  resonator;  B,  the  reed;  C,  the  wind  pipe; 
D,   the  bellows.      (After  Barth.) 

vocal  cords.  When  these  are  approximated  and  air  is  forced  upward 
from  the  lungs  by  means  of  the  diaphragm  and  other  respiratory  muscles, 
the  cords  are  thrown  into  vibration  and  a  sound  is  generated.  The  sounds 
thus  produced  by  the  vocal  cords  and  glottis  pass  upward  through  a 
variable  resonator — mouth  and  nares — and  are  there  modified  as  regards 
their  overtones  by  the  lips,  tongue,  etc.,  and  thus  the  vowel  sounds 
originate.  A  further  modification  of  the  overtones  by  means  of  the 
lips,  teeth,  tongue,  etc.,  results  in  the  consonants  of  articulate  speech. 


PALPATION 


47 


The  laryngeal  sounds  are  further  reinforced  by  means  of  a  large  resonator 
—the  thorax — -which  under  favorable  conditions  vibrates  in  unison  with 
the  larynx  and,  therefore,  amplifies  the  sonorous  waves  and  intensifies 
the  sound,  as  does  a  sound  box  those  of  the  timing  fork.  Vocal  fremitus 
is,  therefore,  not  an  accidental  vibration  of  the  thorax  but  is  a  rhythmic 
vibration  due  to,  and  in  unison  with,  the  vocal  cords.  In  order  to 
produce  vocal  fremitus  we  must,  therefore,  have: 

1.  Functionally  efficient  vocal  cords. 

2.  A  sufficiently  resonant  voice:  the  resonator  (thorax)  must    bear 
definite  suitable  proportions  to  those  of  the  vocal  cords.     The  existence 


Fig.  46. — Illustration:  from  Gerhardt,  showing  a  sensitive  flame  as  affected  by  vibra- 
tions of  different  variety  and  intensity. 

1.  Gas  flame.     The  flame  is  most  sensitive  just  below  the  flaring  point. 

2.  The  same  on  a  rotating  mirror. 

3.  4,  and  5.     The  flame  while  the  vowel  U  is  loudly  pronounced  at  3,  the  mouth;  4,  the  trachea;  5,  on 
the  anterior  chest  wall. 

i  With  right-sided  pleural  effusion  would  get  2  on  the  right,  and  5  on  the  left  side.) 

6.  Vibrations  over  a  femoral  aneurism. 

7.  The  tympanitic  tracheal  tone,  with  a  half-closed  glottis. 

8.  The  tympanitic  tracheal  tone,  with  open  glottis  (rhythmic  vibrations). 

9.  The  resonant  non-tympanitic  note  of  the  chest  wall  (unrhythmic  vibrations). 


of  such  a  favorable  relationship  in  men,  and  its  usual  absence  in  women, 
explains  the  greater  intensity  of  fremitus  in  the  former.  The  great  indi- 
vidual variations  met  with  in  apparently  similar  types  of  individuals 
have  a  like  explanation. 

3.  Open,  patulous  bronchi. 

4.  Comparatively  free  transmission  of  vibrations  from  the  lung  to  the 
chest  wall;  e.g.,  the  interposition  of  liquid,  as  in  the  case  of  a  pleural 


48  THE    EXAMINATION    OF    THE    LUNGS 

effusion,  diminishes  or  obliterates  fremitus,  unless  the  underlying  lung  is 
solidified,  in  which  case  fremitus  remains  present. 

Fremitus  is  Normally  Intense. — (a)  On  the  right  side,  especially  over 
the  upper  lobe,  because  the  trachea  lies  in  immediate  contact  with  the 
apex  of  the  lung,  whereas  on  the  left  side  it  is  separated  by  a  distance  of 
3  cm.  owing  to  the  interposition  of  the  aorta,  internal  carotid  artery, 
esophagus,  lymphatic  and  areolar  tissue. 

(b)  Posteriorly  between  the  scapulas,  because  of  proximity  to  large 
bronchi. 

(c)  In  the  second  right  intercostal  space,  owing  to  the  nearness  of  the 
bronchial  bifurcation. 

(d)  It  is  more  intense  in  the  interspaces  (finger  tips  used)  than  over 
the  ribs. 


■A 


Fig.  47.  Fig.  48. 

Figs.  47  and  48. — Diagrams  drawn  from  radiograms  of  the  bronchi  filled  with  a  fusible 
alloy  showing  the  relation  of  the  bronchi  to  the  chest  wall.  The  right  bronchus  is  larger, 
and  a  more  direct  continuation  of  the  trachea — which  slopes  toward  the  right.  Contrary 
to  what  is  usually  taught  it  is  not  more,  but  less  horizontal  than  the  left.  The  right 
bronchus  gives  off  a  branch  before  it  enters  the  lung.  The  trachea  bifurcates  at  Louis' 
angle  slightly  to  the  right  of.  the  mid-sternal  line.  At  this  point  vocal  fremitus  and 
resonance  are  intense  and  the  breath  sounds  harsh. 

Fremitus  is  Pathologically  Increased. — (a)  Over  pulmonary  consolida- 
tion, because  of  better  conduction  of  the  vibrations  from  the  bronchi 
(see  Chap.  III). 

(6)  In  cases  of  atelectasis,  because  the  bronchi  are  nearer  to  the  chest 
wall. 

(c)  Over  pulmonary  cavities  (as  a  rule)  because  of  surrounding  con- 
solidation. 

Increased  fremitus  is  generally  associated  with  bronchial  breathing  and 
bronchophony.  Of  course,  in  a  given  case  there  may  be  factors  working 
at  variance  with  one  another  as  regards  the  production  of  bronchial 
breathing,  bronchophony  and  increased  fremitus.  While  these  three 
signs  are  of  the  same  diagnostic  importance  we  must  determine  each 
separately. 

Fremitus  is  theoretically  always  diminished  or  absent  over  cavities. 
There  is  little   or   no  fremitus  over  the  trachea,  because  air  does  not 


PALPATION 


49 


transmit  vibratory  waves  appreciable  to  the  hand,  and  because  there  is 
no  reinforcement  by  a  resonator  as  in  case  of  the  thorax.  But  practi- 
cally we  find  fremitus  in  the  majority  of  cases  increased  over  cavities  on 
account  of  (1)  an  overlying  area  of  consolidated  lung,  (2)  transmission 
by  well-organized  fibroid  walls,  (3)  general  sense  of  increased  fremitus 


from  surrounding  consolidated  lung,  in  other  words,  failure  to  localize 
the  fremitus  directly  over  the  cavity. 

Fremitus  is  Normally  Feeble. —  (a)  As  the  result  of  overlying  fat  or 
mammary  glands  (vibratory  reflection). 

(b)  In  women  and  children  because  the  chest,  the  resonator,  is  not  in 
as  favorable  a  relation  with  vocal  cords  as  in  men  and  because  the  voice 

4 


50 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.  50.  Fig.  51. 

Figs.  50  and  51. — The  dots  indicate  the  areas  of  the  chest  over  which  vocal  fremitus  and 
vocal  resonance  are  normally  most  intense.  The  solid  lines  indicate  the  lower  margins  of 
the  areas  over  which  these  phenomena  are  obtainable  (lower  pulmonary  border).  The 
dotted  lines  indicate  the  lower  margin  during  forced  inspiration,  the  lungs  having  expanded 
downward,  filling  the  complemental  space.  Downward  movement  of  the  percussion  reso- 
nance from  the  solid  to  the  dotted  lines  during  inspiration  also  indicates  pulmonary 
expansibility. 


Fig.  52. — Advanced  bilateral  pulmonary  tuberculosis.  Both  upper  lobes  contain 
cavities  of  variable,  but  for  the  most  part  small,  size,  surrounded  by  completely  infiltrated 
lung  tissue.  The  lower  lobes  of  the  lung  are  relatively  uninvolved.  Fremitus  was  much 
increased  over  the  upper  lobes  and  was  associated  with  bronchophony  and  percussion  dul- 
ness,  having,  especially  in  the  left  axilla  (large  cavity)  a  tympanitic  quality.  Clear-cut 
metallic  rales  were  heard,  as  well  as  whispered  pectoriloquy.  The  lower  lobes  yielded  an 
impaired  note  with  diffuse  crackling  rales.  Expansion  over  the  upper  chest  was  almost 
absent. 


PALPATION 


51 


being  higher  in   pitch  the  vibrations  are  more   rapid  and  hence  less 
readily  felt. 

Fremitus  is  Pathologically  Decreased. —  (a)  In  obstruction  of  a 
bronchus — asthma,  compression,  occlusion.  (In  these  cases  it  ma}' 
return  after  coughing.) 

(b)  From  increased  reflection  or  diffusion  (pleural  thickening,  effusion, 
or  pneumothorax). 

(c)  Over  cavities,  not  surrounded  by  consolidation. 

(d)  In  cases  of  dysphonia — weakness  or  paralysis  of  the  vocal  cords. 
Exceptionally  fremitus  may  be  present  over  pleural  effusions;  this  is 

due  to  the  factors  which  have  been  discussed  on  pages  60,  61. 


Fig.  53. — Palpation  furnishes  the  most  satisfactory  method  of  examining  the  liver. 
The  patient  lies  on  his  back  with  the  knees  slightly  flexed,  and  is  told  to  breathe  slowly  and 
deeply  with  the  mouth  open.  If  the  liver  is  enlarged,  or  displaced  downward,  its  margin 
can  be  felt  to  push  against  the  right  hand  during  the  descent  of  the  diaphragm.  The 
examination  is  rendered  more  satisfactory  if  the  examiner's  left  hand  presses  upward  on 
the  posterior  costal  margin.      Splenic  enlargement  may  be  determined  in  a  similar  manner. 


The  most  intense  fremitus  is  encountered  in  robust,  deep-chested 
men.  The  lower  the  pitch  of  the  voice,  the  slower  the  sound  vibrations 
and  the  greater  their  amplitude,  and  hence,  provided  the  thickness  of  the 
chest  wall  remains  constant,  the  more  marked  the  fremitus.  This  is 
especially  the  case  on  the  right  side,  for  the  reasons  already  mentioned. 

Tactile  vibrations  may  also  be  produced  by: 

(a)  Flowing  liquids — thrill. 

(6)  Movements  of  fluid — fluctuation,  succussion. 


52  THE    EXAMINATION    OF   THE    LUNGS 

(c)  Mechanical  friction — friction  fremitus,  pleural  or  pericardial 
fremitus. 

The  costal  and  visceral  pleura?  during  respiration  glide  with  smooth, 
mirror-like  surfaces  over  each  other.  The  greatest  degree  of  excursion 
is  vertical  (3  cm.).  They  also  move  horizontally,  their  motion  being 
downward  and  forward  during  inspiration  (see  Figs.  9,  10,  11).  In 
health  no  palpable  thrill  or  audible  sound  is  produced.  But  the  pleural 
surfaces  roughened  by  disease  may  produce  palpable  vibrations  as  well 
as  sounds  (friction  fremitus  and  friction  sounds),  both  being  most  marked 
in  the  mid-  and  lower-axillary  regions. 


CHAPTER  III 
ACOUSTICS  IN  PHYSICAL  DIAGNOSIS 

For  the  ready  comprehension  of  physical  diagnosis  a  superficial 
knowledge  of  acoustics  is  necessary.  The  phenomena  of  percussion, 
auscultation  and  to  a  considerable  extent  palpation,  cannot  otherwise 
be  grasped  or  properly  interpreted.  We  have,  therefore,  been  led  to 
briefly  review  some  of  the  more  important  laws  of  sound.  Physical  diag- 
nosis is  for  the  most  part  based  upon  a  foundation  of  acoustics.  Our 
interpretation  of  the  signs  elicited  from  both  healthy  and  diseased  tissues 
is  but  a  manifestation  of  the  fact  that  physical  alterations  of  the  tissues 
cause  corresponding  changes  in  the  vibrations  which  they  are  capable  of 
assuming  or  transmitting.  The  fact  that  all  the  phenomena  met  with 
cannot  as  yet  be  satisfactorily  explained  is  due  to  the  limitations  of  our 
knowledge  and  is  not  to  be  attributed  to  any  mysterious  manifestations. 
Acoustics  has  not  developed  into  such  a  lofty,  rich,  well-rounded  form  as 
has  her  sister  science,  Optics. 

Rhythmic  Vibrations. — When  the  equilibrium  of  an  elastic  body  is 
momentarily  displaced,  it  vibrates  back  and  forth  until  its  equilibrium 
is  regained.  Thus  a  bass  viol  string  when  on  a  stretch,  if  plucked,  can  be 
seen  to  vibrate.  The  motion  imparted  to  a  localized  area  is  gradually 
transmitted  throughout  its  whole  length.  The  rate  of  the  vibration  is 
increased  as  the  string  is  rendered  more  taut,  until  separate  vibrations 
can  no  longer  be  seen.  At  the  rate  of  16  per  second  the  lowest  audi- 
ble tone  is  produced.1  For  the  human  ear  the  highest  perceptible 
note  corresponds  to  36,000  vibrations  per  second.  The  vibrations 
are  perceptible  to  touch  (vocal  fremitus)  as  well  as  hearing,  but  touch 
perceives  the  slow,  and  hearing  the  rapid,  vibrations  more  readily.  The 
musical  range  of  vibrations  lies  between  40  and  4000  per  second.  The 
greater  the  tension,  the  more  rapid  the  vibrations,  and  the  higher  the 
pitch.  When  an  elastic  tissue  (e.g.  violin  string),  vibrates  rhythmically 
and  with  sufficient  rapidity  a  tone  is  produced. 

But  a  string  vibrates  both  as  a  whole,  and  simultaneously  in  its  ali- 
quot parts,  at  its  nodal  points,  each  of  which  represents  an  octave  of  the 
fundamental  note  (the  note  of  string  vibrating  as  a  whole).  These  par- 
tial vibrations  produce  additional  tones  which  are  known  as  overtones. 
Overtones  bear  a  simple  relation  to  the  fundamental  note:  2,  3,  4,  5,  7, 
etc.  The  first  six  overtones  are  harmonious,  above  this  they  are  generally 
not  so.  The  combination  of  the  fundamental  note  plus  the  overtones 
produces  what  is  known  as  klang  (timbre).  Klang,  then  (the  musical 
quality)  results  from  rhythmic  vibrations  such  as  occur  when  the  fundamen- 
tal note  vibrates  together  with  harmonious  overtones. 

1  Not  only  the  rate  and  amplitude  of  the  vibrations,  however,  determines  their 
audibility,  their  duration  is  perhaps  of  even  greater  importance.  Recent  investiga- 
tions (Gianfranceschi)  have  shown  that  vibrations  must  last  one-fortieth  of  a  second 
to  be  audible,  and  that  duration  is  a  much  more  constant  factor  in  perceptibility  than 
rate. 

53 


54 


THE    EXAMINATION    OF    THE    LUNGS 


On  different,  though  accurately  attuned  instruments — flute,  violin, 
clarionet — the  same  fundamental  note  may  be  sounded,  yet  the  indi- 
viduality of  each  instrument  remains  distinct ;  we  can  distinguish  one  from 
the  other.  Now  this  individual  difference — timbre,  klang,  quality — is 
dependent  upon  the  character  of  the  overtones.  The  individual  quality 
of  different  voices  is  dependent  upon  similar  factors. 

Unrhythmic  Vibrations. — Theoretically  if  a  string  could  be  struck  at 
a  minute  point,  by  a  hard  hammer,  in  0  time,  the  vibrations  would  tend 
to  remain  localized,  and  those  points  of  the  string  which  had  not  been 
directly  struck  would  begin  to  vibrate  slowly  and  unrhythmically.  As 
a  result  the  overtones  and  especially  the  higher  overtones — the  unhar- 
monious  ones — would  disproportionately  increase  in  strength  and  an 
unpleasant  metallic  note  result  (Helmholtz).  In  the  case  of  the  piano 
this  is  obviated  by  having  the  strings  struck  by  soft  broad  hammers, 


Fig. 


54. — Diagrammatic  illustrations  of  a  vibrating  string.     First,  as  a  whole;  second,  with 
one  nodal  point;  third,  with  two  nodal  points;  fourth,  with  three  nodal  points. 


which  remain  in  contact  long  enough  to  ensure  a  continuous  vibration  of 
the  whole  string,  and  are  so  placed  as  to  dampen  the  unharmonious  over- 
tones by  eliminating  their  nodal  points.  If  in  any  sound-producing  body 
the  elastic  equilibrium  be  briefly  and  locally  disturbed,  unrhythmic 
vibrations  result.  Very  unrhythmic  vibrations  allow  the  distant  overtones 
to  preponderate,  and  a  metallic  quality  is  produced.  This  occurs  regard- 
less as  to  whether  we  are  practicing  auscultation  or  percussion,  and  regard- 
less as  to  whether  these  higher  overtones  are  heard  together  with  the 
fundamental  (amphoric  breathing)  or  separately.  All  the  metallic 
sound  phenomena,  of  auscultation  and  percussion  are  thus  produced 
(metallic  ring,  bell  tympany,  amphoric  breathing,  cracked-pot  sound) 
(see  Fig.  55). 

Vibrations  in  Tense  Membranes. — Tense  membranes  such  as  a 
kettle  drum  or  the  distended  stomach,  tend  to  vibrate  with  very  diverse 
and  variable  nodal  points,  and  hence  the  relationship  between  the  funda- 
mental note  and  the  overtones  is  a  very  variable  one.  This  may  be 
illustrated  by  throwing  stones  into  a  pool  of  water.  Each  stone  will 
produce  its  own  circle  (vibrations)  and  these  circles  will  mingle  and 
interweave  without  losing  the  original  identity. 

Sympathetic  Vibrations. — Vibrations  may  be  set  up  in  neighboring 
tissues  not  only  by  the  direct  conduction  of  the  sound-producing  impact, 
but  also  by  what  is  known  as  sympathetic  vibration.  It  has  been 
stated  that  overtones  accompany  the  fundamental  note,  but  it  is  also 


ACOUSTICS    IN    PHYSICAL    DIAGNOSIS 


55 


true  that  if  an  overtone  be  produced  the  fundamental  note  which  corre- 
sponds to  it  will  begin  to  vibrate.  Thus  if  a  certain  note  on  a  piano  be 
struck  and  suddenly  damped,  certain  other  strings  can  be  heard  to  vibrate. 
If  iodide  of  nitrogen  be  painted  upon  the  "G"  string  of  a  bass  viol  and 
allowed  to  dry,  a  violent  detonation  will  occur  if  a  similarly  pitched 
string  of  another  instrument  in  the  neighborhood  is  set  in  vibration; 
while  vibrations  of  the  "E"  string  are  without  effect.  It  is  also  a  well- 
known  fact  that  the  vocal  or  instrumental  production  of  certain  musical 
notes  may,  to  the  chagrin  of  the  musician,  crack  glass  vases  on  the  nearby 
mantelpiece.  How  important  a  role  sympathetic  vibrations  play  in 
physical  diagnosis  cannot  be  stated,  but  that  they  have  some  bearing 
cannot  be  questioned. 


I\l\l\(\(\l\l\f) 


TWWYAAAA 


/VHWw, 


Rhythmic  vibrations 


Unrhythmic  vibrations 


Very  unrhythmic  vibrations 


or\f\f\  n  n  n  n  n  n  c\  c 

uuuuuuuuuuu 


Loud  sound 

(large  wave  amplitude) 


Feeble  sound 

(small  wave  amplitude) 


n 


01 


Low  pitch 
(slow  vibrations) 


High  pitch 
(rapid  vibrations) 


Fig.  55. — Diagram  illustrating  the  difference  in  the  sounds  produced  by  vibrations  of 

different  kinds. 


Interference  Waves. — When  two  waves  travel  through  a  vibrating 
string  in  opposite  directions,  they  tend  to  nullify  each  other  if  their 
nodal  points  be  similar.  This  phenomenon  has  been  used  to  explain 
some  physical  signs. 

Loaded  Strings. — If  a  piece  of  wax  be  attached  to  one  of  two  tuning 
forks,  or  to  musical  strings  of  a  similar  pitch,  the  vibrations  of  the  struc- 
ture thus  treated  become  slower  than  those  of  its  fellow  and  the  note 
which  it  gives  forth  correspondingly  lower  in  pitch.  A  bottle  filled  with 
soapsuds  gives  forth  a  much  lower  note  when  percussed,  than  a  similar 
body  when  empty.     Here  the  suds  act  as  a  "load"  and  retard  the  vibra- 


56 


THE    EXAMINATION    OF    THE    LUNGS 


tions.  In  lungs  under  normal  tension  the  pulmonary  septa  act  as  a  load, 
and  tend  to  localize  and  delay  the  vibrations.  The  relaxed  lung  in  which 
the  septa  are  no  longer  under  tension  yields  a  tympanitic  note  of  much 
higher  pitch  than  the  normal  organ,  and  vibrates  as  a  whole,  not  merely 
where  it  is  percussed,  as  does  the  normal  lung. 


7Tf  Qvenront 


$  r- 


VOCAL    COR  OS 


Fundamental 


WHEN  THE  SOFT  PALATE  IS  001.™ 
RESOANANCE  CAPACITY  OF  THE  NASAL  CAv 
IS  OBTAINED  WITH  THE  RESULT  THAT  ALl 
THE  OVERTONES  ARE  HEARD  IMPOSED  UPOO 
A  STRONG  FUNDAMENTAL. 


3*0  OVERTONE 


VOCAL  CORPS 


Fundamental 


""— 1  THE  SOFT  PALATE  CLOSES  THE  NASAL  CAVITY  THE 
H  ALONE  ACTS  AS  A  RESONATOR  WITH  THE  RESULT 

[  IS  MARKEDLY,  REDUCED.  THE  FUNOA- 
.ENTAL  TONE  IS  WEAK  AND  SOME  OF  THE  OVERTONES  MAY 
BE  SUPPRESSED. 


Fig.  56. — The  production  of  overtones.  Opposite  the  drawings  are  reproduced  (from 
actualjphotographs  obtained  by  means  of  the  improved  Koenig  manometric  flame  appa- 
ratus) the  vibrations  of  the  fundamental  note  and  the  overtones.  {From  the  ^Scientific 
American.) 


Resonators. — Sound  waves  are  transmitted  readily  from  solid  to 
solid  bodies,  as  from  a  tuning  fork  to  the  skull,  but  not  so  readily  from 
vibrating  bodies  to  the  air — a  violin  string  vibrating  between  the  fingers 
produces  little  sound.  To  increase  the  volume  of  sound,  therefore,  we 
resort  to  the  use  of  sound  boxes  or  resonators,  as  when  a  tuning  fork 
rests  on  a  table.  The  resonators  used  for  musical  instruments  readily 
assume  all  varieties  of  simple  and  compound  vibrations  which  are  im- 


ACOUSTICS    IN    PHYSICAL    DIAGNOSIS  57 

parted  to  them,  that  is  they  vibrate  in  unison  with  the  source  of  the 
sound  (sympathetic  vibration)  and  thus  amplify  the  waves.  Indeed, 
it  is  in  part  due  to  certain  vibratory  habits  which  they  have  acquired 
that  old  violins  owe  their  mellow  richness  of  tone.1 

Resonators  are  also  used  to  analyze  sounds — to  resolve  a  complex 
sound  into  its  component  elements  to  a  degree  which  is  not  otherwise 
possible.  Such  resonators  are  hollow  bodies,  with  a  smooth  lining, 
stiff  walls  and  two  openings.  The  most  powerful  types  are  spherical 
in  shape,  but  many  forms  are  used,  as  in  case  of  the  violin.  For  the 
purpose  of  analyzing  the  sounds  met  with  in  physical  diagnosis,  simple 
telescopic  tubes  2  meters  in  length  have  proved  sufficient.  Resonators 
are  characterized  by  the  fact  that  when  a  sound  is  produced  they  cause 
the  fundamental  note  to  predominate,  while  the  overtones  remain  weak 
and  unharmonic. 

The  large  end  of  the  resonator  is  brought  into  proximity  with  the 
sound  to  be  analyzed,  the  small  end  is  connected  with  the  ear  by  means  of 
rubber  tubing.  By  varying  the  length  of  the  tube  to  the  point  which 
produces  the  loudest  sound  for  a  given  note,  the  wave  length  of  that  note 
can  be  computed  and  its  position  in  the  musical  scale  established. 

In  the  human  body  the  thorax,  a  distended  stomach,  a  pneumo- 
thorax, etc.,  may  act  as  resonators.  The  more  elastic  the  material  of 
which  the  resonator  is  composed,  the  longer  its  vibration.  Thus  a  bell 
sounds  longer  than  a  glass,  and  a  glass  longer  than  a  wooden  bowl. 
A  resonator  15  to  30  cm.  in  length  is  sufficient  to  amplify  the  sound  of 
pure  bronchial  breathing  (little  "D"  to  "E"  on  the  musical  scale),  but 
for  normal  vesicular  breathing  a  length  of  from  1  to  2  meters  ("A"  to 
"F")  is  required.  The  latter  is,  therefore,  from  two  to  three  octaves 
lower  in  pitch  than  the  former.2 

While  inferior  to  the  resonator  in  point  of  accuracy,  very  com- 
plex sounds  can  be  resolved  by  the  human  ear  into  their  component 
elements.  The  expert  leader  can  volitionally  single  out  the  notes  of 
any  individual  instrument  of  his  orchestra,  and  it  is  the  unconscious 
analysis  of  sound — the  separation  of  the  fundamental  note  from  the 
overtones — which  enables  us  to  distinguish  individual  voices,  and  to 
recognize  tympany,  resonance,  metallic  sounds,  etc.,  in  percussion  and 
auscultation.  With  percussion  of  equal  force,  the  high  notes  are  more 
acutely  perceived  by  the  human  ear,  than  the  low  ones,  which  are  apt 
to  be  overshadowed  by  their  overtones.  It  is  evident,  therefore,  that 
the  individual  who  is  the  possessor  of  a  good  musical  ear  will  much  more 
readily  acquire  efficiency  in  auscultation  and  percussion,  and  will  derive 
much  more  information  from  the  employment  of  these  methods,  than  he 
who  is  more  or  less  tone-deaf. 

THE  QUALITIES  OF  SOUND 

The  qualities  of  sound  are  as  difficult  to  describe  as  are  colors  to 
the  blind,  hence  we  are  forced  to  use  similes  and  comparisons.  Sounds 
are  classified  according  to  their  component  qualities,  which  are  intensity, 
duration,  quality  and  pitch. 

1  Wooden  resonators,  especially  those  made  of  spruce  (which  is  made  up  of  very 
long,  straight,  regular  fibers,  and  stretched  taut  like  a  string)  are  chosen  for  most 
musical  instruments,  since  their  vibrations  result  in  much  richer,  mellower  tones  than 
do  those  of  other  wood  or  metal. 

2  Mueller,  F. :  Zeitschr.  /.  Aertzliche  Fortbildung,  ix,  1912,  Xo.  14. 


58  THE    EXAMINATION    OF    THE    LUNGS 

Intensity. — This  depends  upon  the  amplitude  of  the  sound  waves; 
not  only  on  the  force  of  the  blow,  but  also  on  the  number  of  air  columns 
set  in  vibration.     Hence  the  importance  of  percussion  of  equal  force. 

Duration. — The  more  air  in  a  vibrating  column  the  longer  the  dura- 
tion of  the  sound.  The  "fullness"  and  the  "leerness"  of  Skoda,  terms 
which  are  still  occasionally  employed  in  German  literature,  although 
compound  perceptions,  depend  mainly  upon  the  duration  of  the  vibra- 
tions. Resonant  and  tympanitic  notes  are  long;  dull  and  flat  notes  are 
short. 

Quality. — By  this  term  we  mean  that  a  sound  either  is  or  is  not 
musical.  If  it  has  a  musical  quality,  we  say  that  the  sound  possesses 
timbre  or  klang,  attributes  which  depend  upon  the  number  and  quality 
of  the  overtones.  It  must,  of  course,  be  remembered  that  in  physical 
diagnosis  we  shall  find  no  pure  musical  notes,  but  only  varying  degrees 
of  tone  dulling.  The  difference  between  resonance  and  tympany,  be- 
tween a  wooden  bowl  and  a  glass,  is  due  to  the  fact  that  the  last  named 
in  each  instance  possesses  many  and  harmonious  overtones. 

Pitch. — Pitch,  as  was  first  notably  emphasized  by  Austin  Flint,  is 
from  a  medical  standpoint  probably  the  most  important  element  in  the 
analysis  of  sound.  It  depends  on  the  rate  of  the  vibrations — the  more 
rapid  the  rate,  the  higher  the  pitch.  The  longer  the  air  column  set  in 
motion,  the  slower  the  vibration  and  the  lower  the  pitch.  Long  organ 
pipes  or  long  instrumental  strings  of  equal  caliber  give  forth  the  lowest 
sounds.  The  adult  chest  yields  a  lower  note  than  that  of  the  infant. 
Increase  in  pitch,  loss  of  resonance,  and  shortness  of  duration  go  hand 
in  hand  (pulmonary  consolidation).  Auenbrugger  wrote:  "Ubi  sonus 
est  altior,  ibi  est  morbus."  Our  recognition  of  the  degree  of  pulmonarh 
consolidation  depends  largely  upon  the  high-pitched  note  which  sucy 
tissue  yields  when  percussed. 

All  sounds  possess  the  qualities  of  intensity  (loudness)  and  duration, 
some  in  addition  the  qualities  of  pitch  and  tone  (klang). 

In  medical  parlance  we  speak  of  "tones"  and  apply  the  term  to  more 
or  less  distinct  resonances,  but  it  must  be  remembered  that  none  of  them 
are  tones  as  defined  by  physics,  nor  in  the  musical  sense.  In  the  latter 
a  tone  is  a  sound  of  definite  pitch  which  cannot  be  further  resolved  into 
simpler  sounds.  "No  pure  tone  can  have  timbre  (klang)."  Percussion 
sounds  are  always  more  or  less  muffled,  impure  and  dull.  In  a  strict 
sense  there  is  no  sharp  distinction  between  a  noise  and  a  tone.  Each 
can  be  resolved  by  the  ear  into  simpler  tones. 

Extremes  are  easily  recognized,  but  there  are  many  gradations  which  cannot  be 
definitely  analyzed.  Even  the  typical  tympany  of  an  air-distended  abdomen  is 
far  from  having  the  rhythmic  relations  between  the  fundamental  note  and  the  over- 
tones which  is  met  with  in  pure  musical  tones.  Again  tympanitic,  and  non-tym- 
panitic  notes  often  merge  so  gradually  into  each  other  that  an  absolute  differentiation 
is  impossible.  In  the  case  of  a  tympanitic  sound,  the  fundamental  note  is  readily 
appreciable — we  can  sing  it,  but  with  a  non-tympanitic  note  this  is  not  the  case. 
Practically  the  boundary  between  the  two  lies  at  the  point  at  which  the  ear  fails  to 
distinguish  any  one  pitch,  on  account  of  the  interference  of  the  "overtones, "  and  this 
in  turn  is  largely  a  question  of  the  individual  ear. 

For  example,  if  we  strike  a  key  on  the  piano  a  tone  results,  but  if  we  strike  a 
number  of  adjacent  keys,  musical  notes  blend  to  form  a  noise.  Certain  of  the  modern 
"harmonics"  are  mere  noises  to  the  uneducated  ear.1 

1  Geigel:  Deut.  Arch.  f.  kl.  Med.,  vol.  lxxxviii,  p.  598. 


ACOUSTICS    IN    PHYSICAL    DIAGNOSIS  59 

THE  ORIGIN  OF  SOUNDS  HEARD  OVER  THE  CHEST 

The  act  of  speaking  or  breathing  produces  sounds  in  the  upper  respira- 
tory tract — larynx,  vocal  cords,  glottis,  mouth,  nares — which  are  con- 
ducted downward  into  the  chest  mainly  by  the  air  columns  in  the  lumen 
of  the  bronchi.  The  moving  column  of  air  sets  the  pulmonary  tissues 
into  vibration,  and  vibrations  of  certain  kinds  produce  audible  sounds. 

These  sounds  are  conducted  through  the  overlying  tissues  to  the  ear 
of  the  examiner,  and  the  character  of  the  sound  we  hear  depends  upon 
the  character  of  the  tissues  in  their  effect  upon  the  following  acoustic 
factors:  (1)  diffusion,  (2)  absorption,  (3)  reflection,  (4)  resonance,  and 
perhaps  (5)  interference. 

The  Diffusion  of  Sound. — By  this  is  meant  a  loss  of  intensity  due  to 
conduction  over  a  wide  area — a  dilution  of  energy.  In  spreading  from  a 
sphere  of  a  given  size  to  one  double  its  size,  the  intensity  on  the  surface 
of  the  second  sphere,  the  vibratory  energy  per  unit  area,  will  be  halved. 
The  function  of  the  stethoscope  or  of  a  megaphone  is  to  diminish  diffu- 
sion (lateral  radiation) .  Diffusion  appears  to  be  the  most  important  factor 
in  reducing  the  intensity  of  sound  heard  over  the  chest  (Montgomery). 

The  Absorption  of  Sound. — By  this  term  we  refer  to  the  annihilation 
of  sound  as  such,  and  its  conversion  into  forms  of  energy  such  as  heat,  of 
which  the  ear  takes  no  cognizance.  It  plays  but  a  small  role  if  sounds 
travel  such  short  distances  as  is  the  case  in  the  chest.  Its  effects  are  sepa- 
rate and  distinct  from  those  of  diffusion. 

The  Reflection  of  Sound. — Sound  waves  may  be  reflected  backward 
toward  the  direction  from  which  they  come.  This  is  especially  apt  to 
occur  when  vibrations  pass  through  tissues  of  different  densities,  as  for 
instance  when  air-borne  vibrations  pass  from  the  lumen  of  a  bronchus  to 
its  walls  or  from  the  alveoli  to  fluid  or  to  the  chest  wall.  The  degree  of 
loss  of  sound  depends  "upon  the  differences  in  density  and  elasticity  of 
the  two  media,  irrespective  of  whether  the  sound  is  passing  from  the 
heavier  to  the  lighter,  or  from  the  lighter  to  the  heavier  medium,  pro- 
vided the  sound  passes  from  one  medium  to  another  at  the  normal  inci- 
dence, and  provided  that  plane  surfaces  come  into  contact  or  separate 
two  media,  and  provided  that  the  two  media  are  homogeneous  and  infinite 
in  extent"   (Montgomery). 

Resonance. — By  resonance  we  mean  tone  reinforcement,  clue  to  the 
fact  that  amplifying  vibrations  are  set  up  in  a  second  medium  so  that 
the  two  media  vibrate  in  unison  and  a  louder  sound  results. 

Although  playing  a  less  important  role  in  modifying  the  acoustic 
phenomena  in  the  chest  than  do  diffusion  and  reflection,  yet  resonance  at 
times  is  an  important  factor.  It  is  to  be  noted  that  whereas  diffusion, 
absorption  and  reflection  modify  all  sounds  in  like  degree  providing  that 
intensity  is  constant,  resonance  is  selective,  and  amplifies  sounds  of  differ- 
ent pitch  (vibratory  rate)  in  very  different  degree.  "Conditions  favor- 
able to  the  resonance  of  sounds  of  one  pitch  may  actually  diminish  sounds 
of  another  pitch.  In  addition  sounds  from  different  sources  may  come 
together,  and  thus  sounds  will  be  superimposed  upon  one  another,  and  a 
condition  known  as  interference  may  result,"  causing  blurring  of  sound. 
As  an  example  of  this  we  have  the  fact  that  vocal  resonance  may  be 
diminished,  and  yet  the  whispered  voice  sounds  present,  over  a  pleural 
effusion. 


60 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.  A. — Normal  lung.  Reflection  at 
lung-chest  junction,  at  junction  of  tense  mem- 
branous tissues  of  lung  with  air,  and  at  surface 
of  contact  between  bronchi  and  surrounding 
air  in  the  vesicles  (a  somewhat  questionable 
factor).  Diffusion  much  as  in  Fig.  B.  Vocal 
fremitus  and  resonance  normal.  Breath  sounds 
"  vesicular." 


Fig.  D. — Pleural  effusion.  Lung 
air-bearing,  but  membranous  tissue 
relaxed.  Special  reflection  at  lung- 
fluid  junction,  and,  to  some  extent,  at 
surface  of  contact  between  bronchi 
and  surrounding  intravesicular  air. 
Special  diffusion  between  lung  and 
chest  wall.  Vocal  fremitus  and  reso- 
nance diminished.  Breath  sounds 
feeble  or  absent. 


Outer  chest 
surface 


Lung- 
chest-wall 
junction 

Diaphragm 


I  I 


r  /SoLij,     y/\  ^ 


C  |        Trachea 


Bronchus 


Fig.  B. — Solid  lung.  No  special  reflection 
after  the  sounds  enter  the  bronchial  walls. 
Diffusion  an  important  factor,  but  no  special 
diffusion  present  that  is  absent  in  other  condi- 
tions. Vocal  fremitus  and  resonance  increased. 
More  sound  retained  within  the  bronchi  than 
normally.     Bronchial  breathing. 


Fig.  E. — P neumothorax.  Lung 
solid.  Special  reflection  at  air-chest- 
wall  junction  and  lung-air  junction. 
Special  diffusion  between  lung  and  chest 
wall.  Vocal  fremitus,  resonance  and 
breath  sounds  diminished  or  absent. 


Pulmonary 
surface 


-»'» 


!../ 


M 


,     /FLUID 

{     J.-"* -N,        - 

i *_ ^i I 

Fig.  C. — Pleural  effusion.  Lung  solid.  No 
special  reflection.  Special  diffusion  between 
lung  and  chest  wall.  Vocal  fremitus  and 
resonance  may  be  increased. 


i! 

1 1 
1 1 
i  > 


/ 

r 

f\< 

1 

1 

/      i 

\         //I 

1 

/      i 

\     //    1 

1 

/      f 
1      f 
1      f 

AIR 

v-5t-^J 

I 

I 
1 
i 

i 

Fig.  F. — P  neumothorax.  Lung 
air-bearing.  Special  reflection  at  air- 
chest-wall  junction,  and,  to  some  extent, 
at  outer  bronchial  surface.  Special 
diffusion  between  lung  and  chest  wall. 
Vocal  fremitus,  resonance  and  breath 
sounds  diminished. 


ACOUSTICS    IN    PHYSICAL    DIAGNOSIS  61 

The  importance  of  resonance  or  vibratory  amplification  in  regard  to 
vocal  fremitus  has  been  considered  in  the  preceding  chapter. 

"Normal  Lung. — The  diminution  of  sounds  on  their  way  through  the 
normal  chest  is  due  chiefly  to  the  factors  of  diffusion  and  reflection.  The 
latter  acts  particularly:  (1)  As  the  sound  within  the  air  in  the  bronchi 
comes  into  contact  with  the  bronchial  walls,  especially  of  the  larger 
bronchi;  (2)  as  the  sound  passes  from  bronchial  wall  to  the  air  in  the 
surrounding  vesicles;  (3)  as  the  sound  comes  into  contact  with  the  tense 
pulmonary  membranes;  and  (4),  as  the  sound  passes  from  the  air  in  the 
lung  to  the  chest  wall  (Fig.  57,  A). 

"Consolidation. — Apart  from  the  marked  loss  in  intensity  of  the 
sounds  as  they  pass  from  within  the  bronchi  to  the  bronchial  walls,  the 
chief  loss  of  sound  in  consolidation  as  it  passes  to  the  periphery  of  the 
chest  is  due  to  diffusion.  It  is  not  due  to  absorption.  One  can  readily 
see  whv  the  solid  lung  ordinarily  gives  louder  sounds  than  the  normal 
lung  (Fig.  57,  B). 

"Pleural  Effusion. — In  cases  with  diminished  or  absent  vocal  reso- 
nance the  chief  source  of  sound  loss  after  the  vibrations  have  entered  the 
fluid  is  due  to  diffusion,  and  not  to  absorption  or  reflection.  Diminution 
of  sound  is  impeded,  and  there  may  be  an  actual  increase  in  vocal  reso- 
nance when  the  lung,  instead  of  being  collapsed  and  air-bearing,  is  actually 
solid,  because  there  is  comparatively  little  sound  lost  at  the  lung-fluid 
junction  when  the  lung  is  solid,  just  the  reverse  of  what  occurs  when  the 
lung  contains  air  (Figs.  57,  C  and  D). 

"Pneumothorax. — The  conditions  here  are  roughly  parallel  to  those 
encountered  in  pleural  effusion,  provided  the  lung  is  air-bearing  and  is 
equidistant  from  the  chest  wall  in  each  case,  except  that  with  pneumo- 
thorax a  marked  loss  in  sound  intensity,  instead  of  occurring  at  the  lung- 
fluid  junction,  is  met  with  at  the  air-chest-wall  junction.  If  the  lung 
in  the  case  of  pneumothorax  is  solid,  a  very  serious  loss  in  sound  intensity 
will  take  place  at  the  lung-air  junction.  If  an  open  fistula  between  a 
bronchus  and  the  pleural  cavity  exists,  the  vocal  resonance  will  be 
increased"  (Montgomery)  (Figs.  57,  E  and  F). 

The  inspiratory  vesicular  sound  arises  within  the  lungs  at  the  point  at 

which  the  air  passes  from  the  smallest  bronchioles  into  the  alveoli.     It  is 

ordinarily  independent  of  the  sounds  arising  in  the  upper  respiratory  tract. 

The  expiratory  vesicular  sound  arises  partly  if  not  entirely  in  the 

upper  respiratory  tract  (nares,  mouth,  glottis,  larynx)  (Fig.  96). 

The  sounds  which  we  hear  in  bronchial  breathing  arise  mainly  in  the 
upper  tract.  The  solidified  lung,  though  causing  no  new  sounds  may 
modify  those  already  produced  above.  The  same  facts  apply  to  caver- 
nous and  amphoric  breathing;  the  cavities  which  yield  them  modify  an 
already  existent  sound  by  acting  as  resonators.  New  sound  production 
due  to  the  air  entering  or  leaving  an  excavation  is  general^  if  not  always 
a  negligible  factor. 

Fig.  57. — Diagrammatic  representation  of  how  reflection  and  diffusion,  the  most  impor- 
tant factors  that  diminish  sounds  on  their  way  through  the  chest,  may  operate  in  some 
pulmonary  and  pleural  conditions.  (After  Montgomery  and  Eckhardt,  "Pulmonary 
Acoustic  Phenomena,"  10th  Report,  Henry  Phipps  Institute,  Phila.,  1915.) 

The  continuous  lines  indicate  surfaces  of  special  reflection;  the  broken  lines  indicate  the 
surfaces  of  no  special  reflection  except  those  common  to  all  the  conditions,  namely,  the  outer 
chest  surface  and  the  internal  bronchial  surface.  Fluid- tissue  junctions,  and  the  junctions 
between  relaxed  lungs  and  air,  are  not  specially  indicated,  because  the  changes  in  density  at 
these  junctions  are  not  specially  great. 


62  THE    EXAMINATION    OF   THE    LUNGS 

The  preceding  facts  explain  why  the  physical  signs  over  what  appear 
clinically  to  be  identical  conditions  at  times  vary  diametrically.  Thus 
some  cases  of  pleural  effusion  yield  diminished,  or  absent,  fremitus,  vocal 
resonance,  breath  sounds  and  whispered  sounds,  while  in  another  clinically 
identical  case  these  signs  may  not  only  be  present  but  at  times  actually 
increased.  These  discrepancies  are  mainly  due  to  the  fact  that  in  the 
former  instance  the  lung  is  air-bearing — merely  relaxed,  while  in  the 
latter  the  lung  is  solidified,  either  as  a  result  of  compression  or  consolida- 
tion. Analogous  variations  occurring  in  cases  of  pneumothorax  are  to 
be  explained  upon  the  same  basis. 

The  effects  of  these  differences  in  the  density  of  the  tissues  upon  sound 
reflection  and  diffusion  are  accountable  for  the  difference  in  the  findings. 


CHAPTER  IV 
THE  HISTORY  AND  THE  THEORY  OF  PERCUSSION1 

The  theory  of  percussion  is  based  upon  the  fact  that  when  elastic 
matter  which  is  capable  of  adequate  vibration  is  struck,  a  sound  will  be 
produced.  Thus  by  striking  a  blow  on  the  chest  wall  a  sound  is  generated 
which  varies  with  the  character  of  the  tissues  within  the  thorax.  Per- 
cussion although  practised  from  early  Grecian  times  for  the  differentia- 
tion of  ascites  from  tympanites,  was  not  used  for  thoracic  diagnosis  until 
1755.  Leopold  Auenbrugger  (b.  Gratz,  1722)  was,  when  about  thirty 
years  of  age,  put  in  charge  of  a  Spanish  Military  Hospital  in  Vienna,  and 
while  doing  his  duties  there,  invented  the  art  of  percussion." 

The  principles  of  Auenbrugger's  discovery  are  mainly  two:  first, 
that  percussion  sounds  are  simply  manifestations  of  acoustic  phenomena 
which  should  be  expressed  in  corresponding  terms;  second,  that  the  varia- 
tions of  sounds  are  due  to  a  physical  variation  of  the  tissues. 

In  1826  Piorry,  in  Paris,  erroneously  tried  to  establish  the  identity 
of  sounds  as  specific  of  certain  tissues,  e.g.,  a  pulmonal,  cardial,  osteal, 
or  intestinal  note.  The  subject  was  put  upon  a  permanently  fixed  basis 
by  Skoda  of  Vienna,  who  in  1839  wrote:  "  We  must  first  determine  every 
possible  variety  of  percussion  sound  and  ascertain  the  conditions  on  which 
each  variety  depends;  and  then  endeavor  to  reconcile  our  observations 
with  the  well-ascertained  laws  of  sound." 

PERCUSSION  SOUNDS 

If  we  percuss  the  chest  a  sound  will  be  produced,  the  character  of 
which  will  depend  upon  the  amount  of  air,  fluid  and  elasticity  in  the 
lung.  The  sounds  which  are  thus  elicited  are  arbitrarily  classified 
according  to  their  acoustic  properties  as:  (1)  tympany,  (2)  hyper- 
resonance,  (3)  resonance,  (4)  dulness,  (5)  flatness. 

No  sharp  line  of  distinction  can  be  drawn  between  these  sounds. 
They  merge  gradually  into  each  other.  What  for  instance  one  examiner 
might  consider  tympany,  another  of  equal  experience  might  declare  to 
be  hyperresonance.  As  a  general  rule,  however,  distinctions  suffi- 
ciently accurate  for  clinical  purposes,  which  will  be  concurred  in  bjr  other 
reasonably  skilled  examiners,  can  readily  be  established. 

Tympany. — Tympany  is  a  musical  note  in  which,  although  rich  in 
overtones,  the  fundamental  note  can  be  more  or  less  clearly  recognized. 
We  can  sing  a  note  to  correspond  with  its  pitch.  Its  name  is  derived 
from  the  tympanum — kettle  drum.     It  occurs: 

1  Students  and  practitioners  of  medicine  who  are  interested  in  physical  diagnosis 
should  read  the  translation  of  Auenbrugger's  and  Laennec's  articles,  which  are 
readily  available  in  Camac's  "Epoch-making  Contributions  t<>  Medicine,  Surgery 
and  the  Allied  Sciences,"  Philadelphia,  1909;  as  well  as  Flint's  "  Auscultation  and  Per- 
cussion," a  recent  edition  of  which  has  been  revised  by  H.  C.  Thatcher,  M.  D.j 

63 


64  THE    EXAMINATION    OF    THE    LUNGS 

(A)  When  air  in  closed  chambers  vibrates  in  unison  with  an  elastic 
membrane  (in  an  air-filled  stomach  or  intestine). 

(B)  When  air  columns  vibrate  in  smooth-walled  chambers  which 
communicate  with  the  atmosphere  (open  pneumothorax). 

(C)  In  relaxed  lung  tissue  (when  the  lungs  are  removed  from  the 
body,  or  when  their  tension  is  relaxed  by  a  pleural  effusion,  or  by  upward 
displacement  of  the  diaphragm).  The  lung  under  these  conditions 
vibrates  as  a  whole,  not  merely  locally,  the  percussion  stroke  produces 
rhythmic  vibrations.  A  non-tympanitic  note  becomes  tympanitic  when 
the  internal  air  tension  is  relaxed. 

Percussion  of  a  stale  loaf  of  bread  yields  tympany;  of  a  fresh  loaf, 
resonance.  An  air-inflated  bladder  under  moderate  tension  yields  a 
long  tympanitic  sound;  a  tensely  inflated  bladder  gives  forth  a  shorter, 
more  metallic,  less  tympanitic  note. 

"The  tympanitic  character  of  the  note  in  the  first  instance  (A)  is  due  to  the  fact 
that  the  comparatively  relaxed  and  yielding  wall  permits  a  sufficiently  long  duration 
of  the  contact  between  the  wall  and  the  percussing  instrument,  for  the  movement  to 
be  transmitted  to  the  whole  bladder,  so  that  it  vibrates  primarily  as  a  whole,  as  does  a 
string  struck  with  a  cushioned  hammer.  If,  on  the  contrary,  the  bladder  be  markedly 
distended,  contact  is  so  short  as  to  give  rise  to  a  circumscribed  undulation  of  the 
surface,  before  the  movement  has  reached  the  more  distant  parts  of  the  bladder.  In 
this  case  so  many  different  portions  of  the  bladder  vibrate  independently  that  a  vast 
number  of  overtones  are  produced  and  the  sound  is  a  mere  noise"  (Sahli)  (Fig.  58). 

Lungs  removed  from  the  body  yield  a  tympanitic  note,  because  they  have  lost  their 
tonicity  and  diminished  their  bulk.  Pulmonary  tone  is  mainly  due  to  stretched  elastic 
tissue,  but  in  part  to  activity  of  the  bronchial  muscular  fibers.1  Relaxation  or  loss  of 
tone  allows  the  lung  to  vibrate  as  a  whole.  It  is  not  the  air  that  vibrates  as  a  whole, 
because  ligation  of  the  trachea  under  these  conditions  does  not  alter  the  pitch,  nor  yet 
the  elastic  tissue  as  a  whole,  for  this  is  relaxed  and  does  not  vibrate  at  all. 

If  we  reinflate  the  lung  removed  from  the  body  it  becomes  non-tympanitic  (relaxa- 
tion has  given  place  to  tension)  unless  the  lung  be  emphysematous  and  have  lost  its 
elasticity.  This  is  because  with  tension  present,  unrhythmic  vibrations  are  more 
readily  produced,  which  permit  the  overtones  to  predominate  and  render  the  funda- 
mental note  less  perceptible,  and  hence  the  pitch  is  less  recognizable. 

A  lung  section  held  free  in  the  air  gives  a  lower  note  than  when  laid  in  a  plate, 
because  the  weight  of  the  lung  of  itself  causes  an  increase  in  tension.  If  a  lung  be  cut 
in  longitudinal  sections  the  pitch  of  each  will  be  higher,  the  smaller  the  section.  If. 
these  sections  are  again  laid  in  apposition  a  lower  pitch  will  result  than  the  note  of  any 
one.  The  rate  of  vibrations  in  each  section  is  roughly  approximate,  inversely,  to 
the  square  of  the  thickness  (Zamminer  and  Seitz). 

It  is  impossible  either  by  strong  or  light  percussion  to  alter  the  pitch  of  a  tym- 
panitic lung.  The  only  difference  is  that  of  loudness,  because  the  lung  under  these 
conditions  always  vibrates  as  a  whole.  We  must  not  imagine,  therefore,  that  by  light 
percussion  over  a  relaxed  lung,  as  in  pleural  effusion  we  are  eliciting  only  the  note  of 
the  superficial  lung  tissue. 

A  tympanitic  note  is  one  in  which  unrhythmic  vibrations  are  impossible.  It  is 
evident,  therefore,  that  accurate  topographic  percussion  (the  outlining  of  dull  areas) 
is  possible  only  in  the  absence  of  tympany.  This  explains  why  small  broncho-pneu- 
monic areas  or  tuberculous  consolidations  are  so  difficult  to  demonstrate  by  percussion 
in  emphysematous  subjects  in  whom  more  or  less  tympany  is  always  present.  For  a 
similar  reason  dull  areas  in  the  gastro-intestinal  walls,  etc.,  cannot  be  outlined  by 
percussion. 

Tympany  is  normally  heard  on  percussing  the  abdomen,  larynx  or 
trachea,  and  over  the  lower  anterior  and  lateral  margin  of  the  left  lung 
owing  to  the  proximity  of  stomach  and  intestines. 

1  West:  Trans.  Med.  Chir.  Soc,  1898,  p.  273. 


THE    HISTORY    AND    THE    THEORY    OF    PERCUSSION 


65 


Pathologically  tympany  is  heard  : 

1.  In  consolidation  overlying  air  chambers  (bronchi,  cavities) — a 
dull,  high-pitched  tympany. 

2.  Over  cavities  (air-containing  and  at  least  the  size  of  a  walnut)  as 
in  tuberculosis  or  bronchiectasis;  also  often  over  a  pneumothorax. 

3.  Over  relaxed  lung  tissue:  in  the  neighborhood  of  pulmonary  infil- 
trations, and  above  pleural  or  near  pericardial  exudates  (Skodaic  tympany) 
(see  Fig.  320) .  Occasionally  also  in  incomplete  pulmonary  consolidation 
— air  and  fluid,  e.g.,  edema  of  lungs. 

4.  Over  areas  of  subcutaneous  emphysema.  In  such  cases  if  this  con- 
dition overlies  the  lungs,  no  satisfactory  percussion  or  auscultation  data 
regarding  the  state  of  the  lungs  can  be  obtained. 


Fig.  58. — Diagram  to  illustrate  the  difference  in  effect  of  large  and  small  pleximeters,  as 
well  as  of  tense  and  of  flaccid  membranes. 
In  A  the  membrane  is  stiff  and  tense,  the  pleximeter  small,  the  percussion  stroke  staccato.        The 
vibrations  tend  to  remain  localized  and  are  very  unrhythmic,  hence  metallic  sounds  are  produced. 

In  B  the  membrane  is  flaccid,  the  pleximeter  broad  and  the  percussion  blow  of  average  duration. 
The  vibrations  which  result  are  widespread,  as  well  as  rhythmic,  and  hence  the  sound  is  musical  (tym- 
panitic). 

The  pitch  of  tympany  varies,  but  as  a  general  rule,  it  is  higher  than 
that  of  resonance.  Percussion  of  the  stomach,  for  instance,  produces 
very  rhythmic,  regularly  recurrent  vibrations  at  a  rate  of  320  to  450 
per  second.  The  note  is,  therefore,  much  higher  than  that  of  the  lung— 
108  to  54  per  second  (F.  Mueller).  In  either  case  the  pitch  depends 
largely  upon  the  size  and  tension  of  the  organs  in  question. 

Resonance  is  a  long,  clear,  low-pitched  non-tympanitic  sound.  It  is 
due  to  amplification  of  the  sound  waves,  reinforcement  of  tone  (see 
Resonators).  The  percussed  lung  yields  the  fundamental  note  and  the 
thorax  acts  as  the  resonator.  When  the  two  vibrate  in  unison  resonance 
is  produced,  mere  reflection  of  the  waves  is  insufficient.  The  tissues 
must  possess  more  or  less  rhythmic  vibrations  with  the  reflected  waves 
in  order  to  produce  resonance.  Pulmonary  resonance  is  best  elicited  in 
normal  lungs  in  the  left  infraclavicular  region  and  at  the  angles  of  the 
scapulae.  It  has  been  likened  to  the  sound  of  a  drum  covered  by  a 
blanket  (Auenbrugger),  and  to  the  upper  crust  of  a  loaf  of  fresh  bread 
(Flint). 

Resonance  yields  both  a  longer  and  a  louder  note  than  dulness:  R.  0.42,  D.  0.2S 
second.  (Resonance  is  not  due  to  vibrations  in  the  bronchi;  these  structures  may  be 
filled  with  gelatin  and  vet  resonance  persists.  Not  so  the  alveoli.)  The  note  over  a 
normally  distended  healthy  lung  in  the  regions  in  which  it  is  neither  unduly  encroached 
upon  by  organs,  or  overlaid  by  tissues,  is  resonance.  This  can  be  more  or  less  fixed  in 
the  mind  by  frequent  examinations  of  normal  chests,  with  the  reservation,  however, 
£5 


66  THE    EXAMINATION    OF    THE    LUNGS 

that  there  is  no  absolute  normal  standard,  but  merely  relatively  normal  variations. 
In  disease  the  sound  side  if  such  there  be,  must  always  be  compared  with  the  side 
which  is  diseased. 

Selling  has  proved  by  means  of  resonators  that  the  pulmonary  note  is  a  very  com- 
plex one,  made  up  of  many  overtones  of  which  the  lower  ones  predominate.  The  range 
of  pitch  of  normal  resonance  is  from  low  F  to  high  C.  In  healthy  adults  it  goes  down 
to  about  low  A;  in  children  to  middle  F,  in  emphysema  to  low  F.  A  dull  note  on  the 
contrary  is  higher  in  pitch  since  the  deeper  tones  are  subdued  through  the  decreasing 
vibratability  of  the  lung. 

The  upper  range  of  the  pulmonary  percussion  note  represents  the  pleximeter,  the 
lower  range  is  the  lungs'  own  note.  The  latter  varies  with  the  amount  of  air  and 
-  elasticity.  The  fact  that  the  note  between  the  large  right  and  smaller  left  lung  is  not 
more  noticeable,  is  probably  due  to  the  fact  that  when  the  note  is  low,  a  considerable 
difference  in  volume  must  occur  before  an  appreciable  change  of  the  whole  note  is 
produced.  When  infiltration  of  lung  tissue  becomes  complete  we  practically  hear 
only  the  note  of  the  pleximeter  (finger). 

In  the  lungs  the  pulmonary  septa  modify,  the  sound  by  limiting — 
localizing — the  sound  waves;  not,  however,  by  acting  at  nodal  points 
— they  are  too  closely  spaced — but  by  acting  as  a  "  load  "on  a  vibrating 
string  (see  p.  55).  If  the  lung  is  under  normal  tension,  the  vibrations 
remain  localized  in  the  area  percussed.  If  it  is  relaxed,  both  lung  and 
its  contained  air  vibrate  as  a  whole  and  tympany  results. 

Resonance  occurs  only  over  the  lungs  (elastic  air-containing  organs). 
The  larger  the  quantity  of  air,  the  more  resonant  the  note,  especially  if 
its  deep  diameter  lies  in  the  vertical  plane  of  the  percussion  stroke. 

Hyperresonance. — By  this  term  we  understand  a  sound  which 
acoustically  lies  between  resonance  and  tympany,  having  some  of  the 
qualities  of  each  but  failing  to  be  identical  with  either.  It  may  be 
produced  by  percussing  the  normal  chest  during  forced,  deep,  held 
inspiration  (increased  tension,  and  increased  air),  but  is  most  character- 
istically heard  in  cases  of  pulmonary  emphysema  (increased  air  and 
diminished  tension).  The  same  concept  may  be  expressed  by  "resonance 
with  a  tympanitic  quality." 

Dulness. — A  dull  note  is  a  short,  high-pitched,  non-musical  sound. 
Percussion  resonance  disappears  over  the  lung,  and  dulness  takes  its 
place  as  the  result  of  the  following  physical  conditions:  (1)  Absence  of 
tone-producing  material  (consolidation  of  pneumonia,  tuberculosis, 
infarction,  atelectasis).  (2)  Poor  tone  conduction.  (3)  Poor  conduc- 
tion of  the  percussion  stroke  (exudation  between  the  lung  and  the  plexi- 
meter— pleural  thickening,  effusions,  edema  of  the  skin).  Dulness  is 
"the  sound  of  both  fluids  and  solids,  that  of  the  airless  viscera— liver, 
heart,  spleen"  (Da  Costa). 

Pulmonary  dulness  (lack  of  resonance)  indicates  an  abnormally  large 
proportion  of  solids  or  liquids  in  proportion  to  the  amount  of  air  in  the 
pulmonary  vesicles.  With  the  appearance  of  dulness  there  is  always 
an  increase  in  the  elevation  of  the  pitch,  and  an  increased  sense  of  resistance. 
Acoustically,  dulness  is  a  condition  in  which  the  fundamental  note 
preponderates,  and  but  few  overtones  are  heard. 

A  hand  placed  on  a  vibrating  glass  deadens  the  overtones.  Its  musical  quality 
disappears,  we  hear  only  the  fundamental  note.  Air-containing  organs  such  as  the 
intestines  are  more  elastic,  vibrate  more  readily  and  more  complexly,  furnish  more 
overtones  which  produce  a  clearer,  louder,  longer,  higher  pitched,  more  intense  and 
more  musical  sound  (tympany).  Solid  organs  on  the  other  hand — liver,  spleen, 
thigh — yield  but  few  overtones,  hence  the  sound  is  shorter,  weaker  and  more  muffled. 
Percussion  of  normal  lung  produces  a  larger  wave  amplitude — louder  sound — than 
that  of  airless  structures. 


THE    HISTORY    AND    THE    THEORY    OF    PERCUSSION 


67 


The  dull  note  obtained  by  percussing  pulmonary  consolidation  is 
characterized  by  the  predominance  of  high-pitched  sounds,  those  of 
lower  pitch  being  weak  or  inaudible,  and  since  high-pitched  sounds 
fade  out  more  rapidly  than  do  low-pitched  ones,  the  sound  is  not  only 
high-pitched  but  also  short,  and  does  not  carry  far.  The  metallic, 
crackling  rales  heard  in  the  neighborhood  of  pulmonary  consolidation  are 
even  higher  in  pitch  than  the  bronchial  breathing  which  accompanies 
them  (F.  Mueller).     The  normal  lung,  under  normal  tension  (inflation), 


M^-\ 


"" 


Fig.  59. — Showing  different  degrees  of  percussion  dulness  in  a  case  of  pulmonary 
tuberculosis.  The  left  upper  lobe  contains  several  cavities  filled  with  blood  clot  and  sur- 
rounded by  consolidated  lung,  yields  a  very  dull  note.  The  right  upper  lobe  is  diffusely 
infiltrated,  yields  moderate  dulness.  The  left  lower  lobe  is  slightly  infiltrated  and  yields  an 
"impaired  "  note.  The  right  lower  lobe  is  relatively  free  from  disease  and  yields  a  resonant 
note. 

yields  on  percussion,  a  long,  low-pitched,  resonant,  non-musical  note. 
The  pleximeter  finger  recognizes  distinct  elasticity  (normal  resistance). 
The  breath  sounds,  except  near  the  large  bronchi  or  the  trachea,  are 
"  vesicular" — soft,  breezy  and  low  in  pitch.  Expiration  is  much  shorter 
than  inspiration.  Over  the  lower  lobes  the  percussion  note  is  longer  and 
lower-pitched  than  over  the  upper  lobes  because  of  (1)  the  greater  mass 
of  lung  tissue  thrown  ;nto  vibration;  and  (2)  thinner  overlying  tissues. 
The  liver  on  the  right  and  the  stomach  on  the  left  tend  to  add  respec- 
tively a  dull,  and  a  tympanitic,  quality  to  the  lower  pulmonary  margin. 


05  THE    EXAMINATION    OF    THE    LUNGS 

Impaired  resonance  or  impairment  is  a  term  sometimes  used  to  indi- 
cate slight  dulness.  It  is  somewhat  shorter,  high-pitched  and  less 
intense  than  resonance  and  is  produced  by  the  same  causes,  in  lesser 
degree,  which  produce  dulness — slight  pulmonary  infiltration,  etc. 

Flatness  is  a  term  which  is  applied  to  extreme  or  absolute  dulness. 
The  note  of  the  thigh  or  of  a  fluid — pleural  effusion — is  flat.  Some 
physicians  prefer  to  use  the  expressions  slight,  marked  and  absolute 
dulness,  to  those  just  discussed.  Efforts  have  been  made  to  numerically 
classify  or  standardize  different  degrees  of  dulness  as  dulness  number 
1,  2,  3,  4. 

Thus  some  examiners  classify  lack  of  resonance  as  1-  2-  3-  4-line  dulness,  using 
these  terms  to  indicate  respectively  impaired  resonance,  dulness,  marked  dulness 
and  flatness.  This  method  of  recording  has  not  been  satisfactory,  owing  to  lack  of 
standardization.  The  3-line  dulness  of  one  examiner  might  be  called  2-  or  4-line  dul- 
ness by  another.  It  has  been  suggested1  that  since  these  different  degrees  of  dulness 
represent  varying  degrees  of  pitch,  they  might  be  standardized  according  to  a  musical 
scale,  i.e. : 

1.  Normal  resonance  =  F  or   F  sharp  below  middle   C. 

2.  1-line  dulness  =  A    below    middle    C    to    the    latter. 

3.  2-line  dulness  =  E  flat  to  F  above  a  middle  C. 

4.  3-line  dulness  =  B  flat  to  intermediate  C. 

5.  4-line  dulness  =  E-F  above  intermediate  C. 

While  such  standardization  would  be  most  desirable,  we  cannot  but  question 
its  feasibility  especially  among  "non-musical"  examiners. 

MODIFIED  TYMPANY 

The  tympanitic  or  musical  sound  already  described  sometimes  under- 
goes certain  modifications  which  give  it  distinct  and  separate  qualities, 
producing  what  are  known  as  (1)  metallic  ring;  (2)  bell  tympany;  (3) 
cracked  pot  sound.  We  have  already  learned  that  if  vibrations  are  im- 
parted to  an  air-containing  cavity  by  a  steady  stroke  applied  to  a  large 
surface,  rhythmic  vibrations  will  be  set  up  throughout  the  structure. 
If,  on  the  other  hand,  a  quick,  sudden,  localized  blow  be  struck,  the 
vibrations  will  tend  to  remain  localized,  will  be  unrhythmic  and  will 
produce  a  harsh,  metallic,  unpleasant  sound.  This  may  be  illustrated 
by  striking  a  piano  string  with  a  knife  blade. 

The  conditions  necessary  for  the  production  of  markedly  unrhythmic 
vibrations,  and  hence  metallic  sounds  (a  sudden  localized  blow,  and  a 
quick  rebound)  are  most  nearly  fulfilled  in  the  case  of  a  large,  tense, 
superficial  cavity.  Long  before  an  explanation  of  the  genesis  of  these 
sounds  was  forthcoming,  Wintrich  pointed  out  that  metallic  sounds  could 
be  more  easily  demonstrated  by  quick,  forcible  percussion,  and  when  a 
hard,  artificial  pleximeter  was  employed.  To  produce  metallic  sounds 
we  must  have  a  stiff  walled  resonator  which  reflects  better  than  it  trans- 
mits. If  the  cavity  is  deeply  situated,  too  much  lateral  radiation  of  the 
vibrations  will  occur  before  the  cavity  is  reached,  and  vibrations  instead 
of  locally,  will  be  set  up  generally,  throughout  it,  producing  a  tympanitic 
note.  If  the  cavity  is  small,  the  fundamental  vibrations  will  be  very 
rapid,  and  the  overtones  still  more  so.  It  is  possible  that  a  small  cavity 
may  actually  yield  a  metallic  sound  which  we  merely  appreciate  as 

1  Wood,  N.  K. :  "Percussion  of  the  Lung."  Jour.  Amer.  Med.  Assn.,  lxiii,  1914, 
1378. 


THE    HISTORY    AND    THE    THEORY    OF    PERCUSSION  69 

tympany  because  the  unharmonious  overtones  are  above  our  auditory 
range  (36,000  per  second). 

Metallic  ring  is  a  term  which  is  applied  to  a  percussion  note  having 
a  metallic  quality.     It  may  be  heard: 

1.  Over  cavities  not  less  than  4  cm.  in  diameter,  with  smooth,  tense 
walls,  especially  if  superficially  located. 

2.  Over  a  tense  pneumothorax. 

3.  Occasionally  over  intense  apical  infiltration.  In  this  case,  espe- 
cially if  right-sided,  the  trachea  acts  as  the  "  large  cavity  with  tense 
walls." 

4.  At  times  over  a  greatly  distended  stomach. 

Metallic  ring  is  best  heard  with  staccato  percussion  and  if  stetho- 
scopic  auscultation  be  simultaneously  practised. 

Metallic  ring  occurs  only  over  fairly  large  cavities  because: 

1.  Small  cavities  vibrate  too  readily  as  a  whole,  and  because  their 
overtones  are  too  rapid — high-pitched — to  be  perceptible. 

2.  Metallic  ring  is  often  associated  with  a  short,  high-pitched  note 
which  is  closely  allied  to  flatness. 

Examples:  Percussion  of  a  thin  tumbler  yields  tympany.  Percus- 
sion of  a  thick  bottle  yields  metallic  ring.  The  fundamental  note  grows 
deeper  as  the  size  of  the  bottle  is  increased  and  its  opening  diminished. 
The  metallic  quality  is  especially  noted  if  the  ear  be  held  near  to  the 
open  mouth  of  the  bottle  (or  of  the  patient  in  case  of  a  patulous  cavity). 

Percussion  of  a  moderately  inflated  pig's  bladder,  the  cheeks,  or  the 
stomach  yields  tympany;  with  extreme  inflation  the  note  becomes 
metallic. 

Bell  Tympany. — Bell  tympany  is  a  clear,  vibrant,  metallic  sound  which 
may  be  heard  by  ausculting  over  tense  pneumothoraces  while  percussion 
is  practised  on  the  opposite  side  of  the  lung,  using  silver  coins  as  plexor 
and  pleximeter.  A  clear-cut,  slightly  echoing  sound  is  thus  produced 
which  has  been  likened  to  the  sound  of  a  gold  coin  dropped  upon  a 
marble  slab,  or  the  sound  of  a  distant  trolley  bell.  Acoustically  the 
sound  owes  its  character  to  the  fact  that  sustained  high-pitched  overtones 
vibrate  together  with  a  deep  fundamental  note,  and  fade  out  slowly. 
Coins  are  used  for  percussion  since  being  small,  hard  and  metallic  they 
tend  to  impart  unrhythmic  vibrations  to  the  tissues  beneath. 

Cracked-pot  Sound. — This  is  a  metallic  note,  followed  by  a  stenotic 
murmur,  caused  by  the  rapid  expulsion  of  air,  through  a  slit-like  opening, 
as  the  result  of  the  percussion  blow. 

"  Though  obviously  related  to  metallic  resonance,  the  nature  and 
causation  of  cracked-pot  sound  are  essentially  different.  The  expulsion 
of  air  through  a  narrow  opening  plays  a  part  in  causing  it.  Apparently 
the  edges  of  the  opening  are  set  in  vibration,  and  an  opportunity  is  thus 
given  for  the  production  of  high  overtones  by  interference"  (Sahli). 

Cracked-pot  sound  (bruit  de  pot  fele)  then  is  heard:  (1)  when  air  is 
forced  through  a  stenotic  opening  as  in  the  case  of  a  superficial  cavity 
communicating  with  a  bronchus  (vibrations  of  the  tissues  at  the  mouth  of 
the  cavity);  (2)  over  the  chest  of  a  crying  child  (glottic  vibrations);  (3) 
occasionally  over  relaxed  and  infiltrated  lung  tissue.  It  is  most  marked 
if  the  examiner's  ear  be  close  to  the  patient's  open  mouth  and  during 
expiration.  It  is  best  heard  over  a  superficial  cavity  near  the  pulmonary 
apex,  with  tense  but  resilient  walls  and  a  stenotic  outlet.     The  sound 


70  THE    EXAMINATION    OF    THE    LUNGS 

may  be  imitated  by  striking  the  loosely  clasped  hollowed  palms  of  the 
hands  together  against  the  knee,  or  by  suddenly  percussing  a  perforated 
rubber  ball.  All  metallic  sounds  are  best  elicited  if  forcible  staccato  per- 
cussion is  employed. 

Thus  we  find  that:  Rhythmic  vibrations  produce  tympanitic  sounds. 
Unrhythmic  vibrations  produce  non-tympanitic 

sounds. 
Markedly  unrhythmic  vibrations  produce  metallic 
sounds. 


Fig.  60.— The  coin  test. 

Summaey. — 1.  Resonance  is  a  long,  low-pitched,  non-musical  note, 
heard  on  percussing  normal  lung,  due  to  unrhythmic,  more  or  less  local- 
ized vibrations.  It  may  be  imitated  by  percussing  a  loaf  of  fresh  bread. 
It  is  associated  with  a  sense  of  resiliency. 

2.  Tympany  is  a  long  musical  note  of  variable  pitch,  produced  by  per- 
cussing elastic,  air-containing  viscera.  It  is  due  to  widespread  rhythmic 
vibrations  and  may  be  heard  over  the  stomach,  intestines,  over  relaxed 
lung  tissue,  and  over  many  cases  of  pulmonary  cavitation  and  pneumo- 
thorax. It  may  be  imitated  by  percussing  a  loaf  of  stale  bread  or  towel 
folded  many  times  upon  itself,  or  the  inflated  cheeks. 

3.  Dulness  is  a  short,  non-musical,  invariably  high-pitched  sound, 
heard  when  percussing  structures  containing  little  or  no  air.     It  is  due 


THE    HISTORY    AND    THE    THEORY    OF    PERCUSSION  71 


Fig.  61. — Section  through  the  posterior  parts  of  lungs  showing  advanced  pulmonary 
tuberculosis.  . 

The  right  upper  lobe  shows  several  empty  cavities,  one  of  which  is  superficial,  large,  and 
surrounded  by  stiff  fibrous  walls.  High  up  in  the  axillary  region  one  shoulcl  expect  to 
find  metallic  tympany;  amphoric  breathing;  clear-cut,  metallic  rales;  whispered  pectorilo- 
quy, and  if  the  bronchus  leading  into  the  cavity  is  stenotic,  cracked-pot  sound.  ... 

The  left  upper  lobe  shows  diffuse  infiltration  which  would  yield  the  following  physical 
signs:  diminished  expansion,  dulness,  increased  vocal  fremitus  and  resonance,  broncho- 
vesicular  breath  sounds,  crepitant  and  crackling  rales. 

The  position  of  the  liver  and  spleen  in  relation  to  the  chest  wall,  lung  and  stomach  is  well 
illustrated. 


72  THE    EXAMINATION    OF    THE    LUNGS 

to  lack  of  vibratability  and  may  be  imitated  by  percussing  the  inner 
surface  of  the  tibia.  It  is  the  note  heard  over  consolidated  lung  tissue. 
It  has  less  volume  (wave  amplitude)  than  resonance  and  does  not  carry 
far. 

4.  Flatness  is  absolute  dulness.  It  is  a  very  short,  high-pitched  non- 
musical  note,  with  very  little  carrying  power  (intensity).  It  is  heard  in 
percussion  of  viscera  such  as  the  heart  and  the  liver  in  regions  not  covered 
by  lung  tissue  and  may  be  exemplified  by  percussing  the  thigh.  It  is  the 
note  of  liquids  and  is  heard  over  pleural  or  pericardial  effusions.  It  is 
invariably  associated  with  a  marked  sense  of  resistance. 

SPECIAL  PERCUSSION  SIGNS 

Wintrich's  Change  of  Note. — -This  consists  of  a  change  of  pitch  during  percussion, 
which  varies  according  to  whether  the  mouth  be  opened  or  closed,  the  note  being 
higher  in  the  former,  and  lower  in  the  latter  instance.  In  a  pipe  open  at  one  end,  any 
constriction  of  the  opening  lowers  the  pitch  of  the  sound  (Bernoulli).  It  may  be 
demonstrated  by  percussing  the  trachea  with  the  mouth  open,  and  closed.  This 
phenomenon  may  occur  pathologically  if  a  pulmonary  cavity  or  a  pneumothorax 
communicates  with  an  open  bronchus.  It  occurs  rarely  in  pneumonia  and  is  to  be 
explained  by  conduction  of  the  percussion  stroke,  through  the  consolidation  to  a  large 
bronchus.  If  noted  in  recumbency  only,  this  may  be  due  to  temporary  occlusion  of 
the  bronchus  by  fluid.     This  sign  is  of  but  little  practical  value. 

Gerhardt's  Change  of  Note. — This  consists  of  a  change  of  the  percussion  sound, 
with  a  change  of  the  patient's  posture,  and  is  dependent  upon  an  alteration  in  the 
direction  of  the  long  axis  of  a  cavity,  which  contains  both  air  and  fluid.  This  was 
formerly  explained  as  resulting  from  a  change  in  the  length  of  the  air  columns.  This 
is  incorrect  since  the  greatest  possible  differences  in  lung  cavities  are  too  small  to 
account  for  such  changes  in  sound.  The  real  explanation  must  be  sought  in  the  change 
in  tension  which  as  a  result  of  the  contained  fluid,  the  cavity  undergoes  (Geigel). 

Friedreich's  Change  of  Note. — This  phenomenon  consists  of  a  lowering  of  the  pitch 
of  percussion  note  over  a  cavity  during  forced  inspiration,  due  to  an  increased  volume 
of  air.     It  is,  therefore,  supposed  to  indicate  a  patulous,  flexible  cavity. 

Biermer's  Change  of  Note. — This  phenomenon  is  practically  the  same  as  Ger- 
hardt's, except  that  the  former  described  the  metallic  resonance  sometimes  heard  over 
a  pneumothorax.  The  pitch  is  lower  on  sitting  up,  due  to  an  increased  volume  of  the 
pleural  cavity,  caused  by  a  sagging  of  the  diaphragm  owing  to  the  weight  of  the 
effusion. 

None  of  the  foregoing  changes  of  note  are  of  much  practical  importance.  They 
are  rarely  demonstrable,  and  even  when  so  are  often  of  doubtful  significance. 

The  Lung  Reflex. — Local  irritation  of  the  skin,  by  cold,  mustard,  or  continued 
percussion,  may  temporarily  produce  a  reflex  dilatation  of  the  subjacent  lung  tissue 
— a  relative  emphysema — which  may  be  sufficient  to  obscure  slight  degrees  of  per- 
cussion dulness.  Thus  too-prolonged  percussion  of  a  pulmonary  apex  may  tem- 
porarily cause  the  disappearance  of  a  slight  impairment  of  resonance  which  was 
readily  demonstrable  at  the  beginning  of  the  examination.  It  should  not  be  forgotten, 
however,  that  aural  fatigue  on  the  part  of  the  examiner  may  account  for  a  similar 
result.  When  such  an  occurrence  is  suspected,  the  examiner  may  proceed  to  some 
other  step  in  the  examination  and  revert  to  the  examination  of  the  doubtful  region 
after  some  time  has  elapsed. 


CHAPTER  V 
ANATOMIC  CONSIDERATIONS 

The  right  ribs  are  longer,  the  right  lung  larger  (but  shorter),  the  right 
shoulder  often  lower  and  narrower,  the  right  breast  is  higher  and  further 
from  the  mid-sternum,  than  the  left. 

The  Lungs. — The  apices  extend  from  1  to  l1^  inches  (2.5  to  4  cm.) 
above  the  clavicles.  The  right  apex  is  slightly  smaller  than  the  left,  its 
conical  shape  is  due  to  encroachment  of  the  right  innominate  vein.  This 
vessel,  unlike  the  left,  pursues  an  almost  vertical  course,  and  with  the 
superior  vena  cava,  occupies  the  space  which  on  the  left  is  filled  by 
the  anterior,  inner  margin  of  the  pulmonary  apex.  In  addition  to  this  the 
subclavian  artery  pursues  a  course  more  anterior  and  less  mesial,  to  the 
right  apex  than  the  left.  The  left  apex  is  more  dome-like  and  slightly 
larger.  There  is  practically  no  difference  in  the  height  of  the  apices 
on  the  two  sides. 

The  -percussion  note  from  the  right  upper  apex  to  the  second  interspace 
is  slightly  higher-pitched,  less  resonant,  and  at  tim.es  has  a  slightly  tympanitic 
quality  because :  (1)  The  right  apex  is  smaller.  (2)  The  superior  vena  cava 
lies  in  front  of  the  inner  part  of  it,  (3)  The  right  subclavian  artery 
occupies  a  more  anterior,  the  left,  a  more  mesial  position.  These  con- 
ditions account  for  the  diminished  resonance  and  higher  pitch.  (4) 
The  right  apex  lies  in  immediate  contact  with  the  trachea  (Figs.  49, 
52,  76,  77,  97) .  This  accounts  for  the  tympanitic  element  and  in  part  for 
the  elevation  of  pitch.  (5)  A  slight  influence — with  light  percussion — is 
sometimes  exercised  by  increased  thickness  of  the  right  pectoral  muscles. 

SURFACE   LANDMARKS,   ETC. 

The  Right  Lung  The  Left  Lung 

Turns  out  at  the  6th  costo-sternal  articu-     Turns  out  at  the  4th  costo-sternal  articu- 
lation (sternal  line).  lation. 

Turns  out  at  the  5th  costal  space. 
Crosses  the  6th  and  7th  intercostal  space     Crosses  at  the  5th  costal  space, 
(mid-clavicular  line).  Turns  out  at  the  6th  costal  space. 

Crosses  the  6th  and  7th  costal  space. 
Reaches  8th  rib  in  axillary  line.  Reaches  the  8th  in  the  axillary  line 

Reaches  10th  rib  in  scapular  line.  Reaches  the  lower  border  of  10th  dorsal 

Reaches  upper  border  of  the  10th  dorsal         vertebrae  in  scapular  line, 
vertebra. 

Louis'  angle1  (the  junction  of  the  manubrium  with  the  gladiolus) 
marks  the  sternal  attachment  of  the  second  rib.     It  is  opposite  to  the 

1  Louis'  angle,  not  Ludwig's  angle.  It  was  not  described  by  Ludwig,  the  German, 
but  was  named  after  Louis,  the  great  French  clinician,  Ludwig  being  the  German  for 
Louis.  The  angle  was  originally  described  by  Louis  as  a  unilateral  prominence  of 
the  ribs  noted  in  certain  cases  of  emphysema  on  the  most  affected  side. 

(E.  H.  Goodman:  "Historical  Note  on  the  So-called  Ludwig's  Angle  or  Angle  ot 
Louis."     Medical  Record,  July  23,  1910.) 

73 


74 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.  62. — Mediastinal  surface  of  lungs  hardened  before  removal.  This  photograph 
shows  (a)  the  groove  produced  in  the  right  apes  by  the  trachea;  (6)  the  relatively  anterior 
position  of  the  vessels  on  the  right  side;  and  (c)  the  smaller  size  of  the  right  apex.  AG, 
azygos  groove,  VG,  grooves  for  superior  vena  cava,  innominate  vein,  and  subclavian  vessels; 
TG,  tracheal  groove;  SG,  subclavian  groove;  AAG,  aortic  groove;  CI,  cardiac  impression. 


Fig.  63. — Lateral  view  of  lungs  hardened  before  removal.     This  photograph  shows  the 
deeper  vascular  groove  and  the  smaller  size  of  the  right  apex  as  compared  with  the  left. 


ANATOMIC    CONSIDERATIONS 


75 


Fig.  64. — Anterior  view  of  lungs  hardened  before  removal.  This  photograph  shows 
the  anterior  position  of  the  groove  for  the  subclavian  vessels  on  the  right  side,  compared 
with  the  more  superior  position  on  the  left.      SG,  subclavian  groove. 


Fig.  65. — The  lungs  normally  meet  and  frequently  overlap  at  Louis'  angle.  This 
previously  hardened  dissection  shows:  an  infant's  chest,  displaying  a  shrunken  thymus 
gland  between  the  apices  of  the  lungs.      (Fetlerolf  and  Gitlings.) 


76 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.   66. 


-Showing  prominent  angle  of  Louis,  also  small  areas  of  absolute  cardiac  and 
hepatic  dulness  in  a  case  of  emphysema. 


Fig.  67. 


Fig.  68. 


Figs.  67  and  68. — The  solid  lines  indicate  the  position  of  the  pulmonary  margms  ancj  0f 
the  interlobar  fissures.  The  dotted  lines  mark  the  anterior  and  lower  confines  of  the  pleural 
cavities — -the  spaces  into  which  the  lung  expands  during  forced  inspiration.  This  space  at 
its  lower  margin,  which  is  bounded  by  the  diaphragm  on  the  inside  and  the  thoracic  wall  on 
the  outside,  is  known  as  the  complemental  space  of  Gerhardt.  It  is  in  this  space  that  small 
pleural  effusions  first  accumulate,  thus  causing  the  disappearance  of  the  diaphragmatic 
shadow  (see  p.  28),  slight  dulness  on  percussion  and  diminished  vocal  fremitus,  reso- 
nance and  breath  sounds. 


ANATOMIC    CONSIDERATIONS 


77 


level  of  the  fifth  thoracic  vertebra,  indicates  the  level  at  which  the  trachea 
bifurcates,  and  anteriorly  the  upper  point  at  which  the  lungs  meet,  to 
diverge  again  at  the  fourth  costal  cartilage.  It  marks  the  upper  boundary 
of  the  cardiac  auricles,  and  the  point  at  which  the  veins  of  the  hand  col- 
lapse while  the  arm  is  being  raised  upward  from  its  lowest  to  its  highest 
position  (Gaertner's  test  of  venous  blood  pressure).  It  forms  a  con- 
venient landmark  from  which  to  count  ribs. 


Fig.  70. 

Fig.  69. — An  approximate  knowledge  of  the  location  of  the  pulmonary  fissures  is  espe- 
cially important  in  the  diagnosis  of  interlobar  empyema.  Right  lung.  The  fissure  between 
the  upper  and  the  lower  lobe  corresponds  to  a  line  drawn  from  the  fourth  dorsal  vertebra  to 
the  fifth  or  sixth  costo-sternal  articulation.  The  upper  border  of  the  middle  lobe  is  marked 
by  a  line  drawn  from  the  middle  of  that  just  described,  to  the  third  costo-sternal  articula- 
tion.     {After  Doyen,  Bouchon  and  Doyen.) 

Fig.  70. — Left  lung.  The  interlobar  fissure  may  be  located  by  drawing  a  line  from  the 
fourth  dorsal  vertebra  to  the  sixth  costo-sternal  articulation.  These  relations  are  not  ab- 
solutely fixed,  but  are  subject  to  individual  variations.      {After  Doyen,  Bouchon  and  Doyen.) 


The  vertebral  spines  correspond  to  the  level  of  the  rib  below.  The 
first  rib  begins  and  is  in  direct  articulation  with,  the  seventh  cervical 
vertebra.  The  second  rib  articulates  with  the  second  and  third  verte- 
brae, the  third  rib  with  the  third  and  fourth  vertebrae,  etc.,  but  the 
eleventh  and  twelfth  ribs  articulate  directly  with  their  respective  verte- 
brae. The  scapulce  overlie  the  second  to  the  seventh  or  the  third  to 
the  eighth  ribs.  The  hilus  of  the  lung  lies  opposite  to  the  spines  of  the 
fourth,  fifth  and  sixth,  and  the  bodies  of  the  fifth,  sixth  and  seventh, 
vertebrae. 


78 


THE    EXAMINATION    OF   THE    LUNGS 


Fig.  71. — Vertical  section  of  the  body,  showing  the  shape  of  the  lower  lobes,  the  upper 
lobes  having  been  removed.  Note  the  higher  position  of  the  right  phrenic  dome,  which 
causes  the  lower  border  of  pulmonary  resonance  to  be  slightly  higher  on  the  right  side.  On 
the  left  the  stomach  imparts  a  tympanitic  quality  to  the  lower  portion  of  the  lung.  If 
filled  with  food  it  diminishes  pulmonary  resonance  and  may  simulate  consolidation  or  a 
small  pleural  effusion. 


CHAPTER  VI 
METHODS  AND  RESULTS  OF  PERCUSSION 

The  Immediate  or  Direct  Method. — The  hand  or  the  finger  tips  are 
struck  directly  against  the  object  in  which  we  desire  to  set  up  vibrations. 
This  was  the  method  of  Auenb rugger,  who,  however,  covered  the  fingers 
with  a  soft  glove  to  diminish  the  finger  element  of  the  sound,  especially 
the  overtones.  The  direct  method  is  still  occasionally  employed  to 
determine  the  resonance  of  the  upper  lobes  of  the  lung  (by  using  the 
clavicle  as  the  pleximeter),  or  that  of  the  lower  lobes  as  a  whole,  by 
striking  the  patient's  back  with  the  edge  of  the  hand. 

The  Mediate  or  Indirect  Method. — This  was  suggested  by  Piorry, 
who  interposed  a  hard  object — the  pleximeter — between  the  plexor  (the 
object  striking  the  blow)  and  the  part  to  be  percussed. 

Artificial  plexors  and  pleximeters  are  sometimes  used,  especially  for 
class  demonstration.  They  generally  consist  respectively  of  a  small 
light  rubber-tipped  hammer,  and  of  a  narrow  piece  of  bone  or  vulcanite 
of  variable  shape  (Fig.  72) .  The  fingers  are  nearly  always  used  as  plexor 
and  pleximeter. 

The  middle  finger  of  the  left  hand  is  pressed  firmly  against  the  chest 
wall,  in  a  direction  parallel  to  the  ribs,  while  the  middle  finger  of  the  right 
hand  strikes  upon  it,  just  behind  the  nail,  a  short,  light,  quick,  vertical 
blow,  delivered  from  the  wrist  (Figs.  73  and  74). 

The  Pleximeter. — Despite  the  fact  that  a  hard  pleximeter,  a  quick 
rebound  and  a  short  time  of  impact  are  advantageous,  we  cannot  use 
an  unpadded  plexor  of  hard  material  because  in  such  a  case  a  high-pitched 
sound  would  be  produced,  due  to  the  overtones  of  the  pleximeter  which 
would  overshadow  the  low-pitched  fundamental  note  of  the  lung.  We 
therefore  use  a  soft  plexor  or  the  finger,  just  as  we  use  felt  pads  in  a  piano 
in  order  to  let  the  basic  note  preponderate  and  to  drown  out  the  unhar- 
monious  overtones.  The  vibrating  area  equals  in  size  the  percussed  area 
plus  a  radiation  during  the  course  of  transit.  Hence  the  smaller  the 
pleximeter  and  the  more  superficial  the  tissue  percussed,  the  more  accurate 
our  topographic  results  (see  Fig.  75). 

Half  the  diameter  of  the  pleximeter  must  always  be  allowed  as  the 
unavoidable  margin  of  error  in  estimating  the  boundaries  between  an 
■ air-containing  and  an  airless  structure  as  the  heart  and  lung,  even  when 
the  pleximeter  is  applied  in  a  direction  parallel  to  the  anticipated  bound- 
ary line.  Based  upon  these  facts  some  very  narrow,  wedge-shaped  plex- 
imeters (Ziemmsen)  have  been  devised  for  limiting  the  lung  apices,  cardiac 
boundaries,  etc.  The  results  derived  from  their  employment,  however, 
have  been  disappointing  (Fig.  72). 

The  percussion  blow  may  be  delivered  either  lightly  or  forcibly,  and 
accordingly  we  speak  of  light  or  heavy — superficial  or  deep — percussion. 
The  latter  terms  are  used  because  with  heavy  percussion  a  deeper  pene- 
tration of  the  vibrations  is  ensured — the  sphere  of  the  blow  is  larger — 
greater  masses  of  tissue  are  set  in  vibration  and  a  louder  sound  is  produced. 

79 


80 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.  72. — 1,  Plexor  or  percussion  hammer;  2,  ivory  pleximeter;  3  and  4,  Hirschfelder's 
pleximeter;  5,   Sansom's  pleximeter. 


Fig.  73. 


Fig.  74. 


Figs.  73  and  74. — The  method  of  percussion.  The  percussion  blow  is  struck  from  the 
wrist  only,  the  forearm  being  practically  stationary.  The  impact,  which  is  delivered  just 
behind  the  nail  of  the  middle  finger,  should  be  quick  and  brief  in  duration,  the  force  of  the 
blow  should  fall  as  vertically  as  possible.  Fig.  73  shows  the  beginning,  Fig.  74  the  end 
of  the  percussion  stroke.  In  order  to  deliver  a  vertical  blow  with  the  terminal  phalanx,  the 
nail  of  the  second  finger,  which  is  generally  used  as  plexor,  must  be  short. 


METHODS    AND    RESULTS    OF    PERCUSSION  81 

The  fingers  are  preferable  to  artificial  plexors  and  pleximeters 
because  of  the  important  information  derived  from  the  sense  of  resist- 
ance. It  is  a  relatively  easy  task,  for  one  practised  in  percussion, 
to  outline  accurately  dull  areas  by  this  means  alone.  It  is  a  useful  method 
when  we  are  forced  to  make  our  examination  in  the  presence  of  extraneous 
noise. 

THE  RESULTS  OF  PERCUSSION 

As  the  result  of  a  percussion  stroke  on  the  chest  wall,  the  equilibrium 
of  the  underlying  tissues  is  locally  disturbed,  they  are  thrown  into  vibra- 
tion, and  a  sound  results.  This  sound  is  produced  by  vibrations  arising 
from  three  sources: 

1.  From  the  Pleximeter. — This  element  of  the  composite  sound  is 
high-pitched,  of  short  duration  and  dull. 

2.  From  the  Thoracic  Wall.— This  element  also  yields  a  short,  dull, 
high-pitched  (osteal)  note.  When  the  costal  cartilages  are  ossified  much 
of  the  percussion  blow  is  absorbed  by  the  arch-like  structure  of  the  ribs, 
penetration  is  diminished,  and  a  more  or  less  tympanitic  note  is  produced. 

3.  From  the  Underlying  Tissues  (Lungs,  etc.). — That  portion  of  the 
sound  which  is  contributed  by  the  vibrations  of  a  healthy  lung  under 
normal  tension  is  long,  low-pitched  and  resonant,  because  of  the  thin- 
ness and  elasticity  of  the  pulmonary  tissue,  and  the  large  amount  of  air 
it  contains.     The  greater  the  depth  of  the  lung,  the  lower  the  note. 

Sound  travels  radially  from  point  struck  and  gradually  fades.  It  is 
conducted  through  tubes  (bronchii,  stethoscope)  to  much  greater 
distances  because  lateral  radiation  is  minimized. 

Sound  waves  in  traveling  through  the  body  meet  with  media  of 
varying  density  and  are  in  part  (a)  reflected;  (b)  transmitted  (by  setting 
up  vibrations  in  the  second  medium).  In  passing  through  media  of 
different  densities  much  sound  is  lost  by  reflection. 

In  percussing  the  chest  the  overlying  tissues  in  different  symmetrical 
regions  are  much  the  same  (skin,  fat,  bone,  etc.)  and,  therefore,  com- 
parisons of  the  underlying  tissues  can  readily  be  made.  But  when  fat 
or  edema  are  excessive,  percussion  data  are  obtained  with  difficulty. 

Sound  is  conducted  better  if  its  waves  impinge  vertically  upon  the 
dividing  point  of  two  media  than  if  they  reach  it  obliquely.  Hence  the 
percussion  stroke  must  fall  vertically  in  order  to  penetrate  deeply. 

Although  percussion  sets  up  vibrations  in  the  entire  lung,  yet  it  does 
so  in  the  deeper  portions  insufficiently  to  set  up  audible  sounds.  Prac- 
tically, therefore,  in  case  of  a  normally  distended  lung  with  light  or  moderate 
percussion,  the  vibrations  tend  to  remain  localized  both  as  regards  lateral 
radiation  and  vertical  penetration. 

It  has  been  shown  orthodiagraphically  that  the  heart  may  be  accurately  outlined 
both  by  forcible  and  by  very  light  percussion.  It  was  questioned  whether  threshold 
percussion  had  sufficient  penetration  to  traverse  the  lung  overlying  the  heart  or 
whether  the  alterations  of  sound  were  not  simply  the  result  of  altered  pulmonary 
tension  due  to  the  nearby  solid  organ.  Weil's  statement  made  years  before  and 
generally  accepted  was  to  the  effect  that  percussion  vibrations  penetrated  only  5 
to  7  cm.,  thus  only  4  to  5  cm.  into  the  lung  itself.  This  belief  was  founded  on  the  Eacl 
that  liver  dulness  could  not  be  demonstrated  when  more  than  4  to  5  cm.  of  lung  1  issue 
overlay  it.  The  following  experiments  show  that  even  light  percussion  has  a  deep 
penetration. 

I.  Moritz  and  Rihl  beat  up  into  a  spongy  froth,  a  solution  of  stiffening  gelatin  to 
which  formalin  and  carbolic  acid  had  been  added,  this  closely  resembling  lung  t  issue  in 
6 


82  THE    EXAMINATION    OF    THE    LUNGS 

structure.  This  was  poured  into  a  glass  cylinder  4  cm.  in  width  and  70  cm.  in  length. 
Before  the  gelatin  had  "set"  a  small  rubber  balloon  was  placed  in  its  midst,  not  in 
contact  with  the  glass,  and  connected  by  means  of  a  tube  with  a  sensitive  flame.  The 
lightest  possible  percussion  produced  vibrations  in  the  flame. 

II.  A  cylinder  20  by  20  cm.  gave  the  same  tone  whether  light  or  heavy  percussion 
was  used,  showing  that  in  either  case  the  same  mass  of  air  vibrated. 


Fig.  75. — Diagram  illustrating  the  penetration  of  audible  percussion. 

1.  Very  heavy — 3  finger  or  fist  percussion — at  P  produces  audible  vibrations  throughout  the  triangle 
a'Pb'.     This  tends  to  bring  out  the  note  of  the  lung  as  a  whole. 

2.  Heavy  percussion  atP  sets  up  audible  vibrations  throughout  the  triangle  aPb. 

3.  Average  percussion  atP'  sets  up  audible  vibrations  throughout  the  area  C'P'D' . 

4.  Light  percussion  at  P'  causes  audible  vibrations  only  throughout  the  area  CP'D. 

III.  Wintrich  showed  that  percussion  of  the  clavicles  in  the  corpse  was  readily 
palpable  by  the  hand  held  beneath  the  diaphragm.  Here,  of  course,  bony  conduction 
also  occurred. 

IV.  If  lung  tissue  be  immersed  in  water  whose  surface  is  percussed,  the  pulmonary 
resonance  can  be  elicited  if  percussion  be  performed  directly  over  the  lung,  but  not  if 
the  stroke  is  delivered  beyond  its  margin.     But,  of  course,  percussion  vibrations  are 


METHODS    AND    RESULTS    OF    PERCUSSION  83 

more  directly  conducted  by  water  than  by  air  or  lung  tissue,  especially  when  in  case 
of  the  latter  the  bony  thoracic  arch  is  interposed. 

V.  Moritz  and  Rihl  further  showed  by  modifications  of  the  gelatin  experiment  and 
by  attention  to  physical  laws  such  as  that  regarding  the  parallelogram  of  force,  that 
the  laterally  radiating  percussion  waves  in  media  denser  than  air  lose  much  of  their 
penetration  power. 

An  ovoid  cylinder  yields  a  lower  note  when  percussed  in  the  direction  of  its  long 
axis. 

It  is  evident,  therefore,  that  the  physical  character  of  lung  tissue  is  such  that  a 
vibration  of  the  entire  mass  always  occurs  even  with  the  lightest  percussion.  Never- 
theless it  reacts  to  percussion  in  such  a  manner  that  a  louder  note  is  produced  when  a 
larger  mass  of  pulmonary  tissue  is  directly  exposed  to  the  impact  than  when  only  a 
thin  layer  of  lung  tissue  underlies  the  area  of  the  percussion  blow.1 

The  following  points,  therefore,  deserve  to  be  emphasized.  Light 
percussion  is  essential  for  topographic  diagnosis;  with  heavy  percussion  too 
much  lateral  radiation  occurs.  Heavier  percussion  must  be  used  where 
the  superficial  tissues  are  thick,  in  order  to  set  up  audible  pulmonary  vibra- 
tions, but  at  the  same  time  the  accurate  delimitation  becomes  more  difficult. 
Very  heavy  percussion  may  give  us  a  general  idea  as  to  the  amount  of  air- 
bearing  tissue  in  the  lung  as  a  whole.  It  is  absolutely  useless  for  the  purpose 
of  outlining  of  organs. 

For  practical  purposes  then,  in  so  far  as  audible  sound  production  is 
concerned,  the  penetration  of  the  percussion  wave  is  about  6  cm.  (2% 
inches).  Of  this,  2  to  3  cm.  is  consumed  in  penetrating  overlying  tissues 
so  that  only  3  or  4  cm.  (1^  inches)  are  left  to  enter  the  underlying  organ. 
Hence  percussion  is  practised  from  all  directions.  The  heart  could  not 
be  outlined  from  behind,  nor  deeply  placed  pulmonary  lesions  from  in 
front.  The  fact,  however,  that  consolidations  the  size  of  a  cherry,  and 
deeper  than  2%  inches  cannot  be  located  by  light  percussion  does  not 
prove  that  sound  waves  may  not  penetrate  deeper.  Deep  percussion 
tends  to  bring  out  note  of  lung  in  its  entirety,  and  drowns  out  slight  degrees 
of  dulness. 

For  light  percussion  the  pleximeter  must  be  lightly  but  snugly 
applied  to  the  chest  wall,  the  stroke  must  be  gentle  and  its  duration 
short,  so  as  to  include  only  a  small  sphere  of  blow  (Fig.  75).  We  should 
percuss  so  as  to  evoke  practically  no  note  over  the  dull  areas.  Light  per- 
cussion is  more  accurate  because  with  it  there  is  less  lateral  radiation. 
For  deep  percussion  the  plexor  is  applied  more  firmly,  the  blow  is  some- 
what longer  and  more  intense.  Too  strong  a  blow  is  transmitted  too 
far  laterally  and  renders  exact  localization  impossible.  Deep  percussion 
is  not. necessarily  loud  percussion.  Percussion  should  be  of  such  strength 
and  duration,  as  to  make  the  difference  between  resonance  and  dulness  as 
great  as  possible. 

"  The  deep  dulness  of  organs  depends  only  on  the  volume  of  the  air- 
containing  parts  in  the  region  of  the  sphere  of  the  blow"  (Weil)  and  not 
as  was  formerly  taught  upon  the  dulling  influence  of  the  neighboring- 
solid  organs  upon  those  filled  with  air.  Such  a  dulling  influence  does  not 
exist  (Sahli).  The  strength  of  percussion  must  vary  with  the  size  and 
character  of  the  organs  and  neighboring  tissues:  e.g.,  in  children  (thin 
chest  walls,  superficial  organs)  light  percussion  is  necessary;  in  corpulent 
adults  (thick  chest  walls,  deeply  placed  organs)  heavier  percussion  is 
required. 

1  Moritz  and  Rihl:  Dent.  Arch.  f.  kl.  Med.,  1909. 


84 


THE    EXAMINATION    OF    THE    LUNGS 


As  has  been  stated,  the  percussion  note  obtained  over  the  lung  is  a 
compound  sound,  consisting  of  the  note  of  the  pleximeter,  the  chest  wall, 
and  lung.  In  heavy  percussion  it  is  the  lower,  and  in  light  percussion 
the  higher,  range  of  this  complex  to  which  our  chief  acoustic  attention  is 
directed.  Both  have  the  higher  range — the  pleximeter  note — in  com- 
mon, but  there  is  relatively  more  of  the  pleximeter  note  in  the  sound 
produced  by  light  percussion.  Lessening  of  the  amount  of  pulmonary 
air  is  manifested  by  a  lack  of  the  deeper  tones. 


4*i^ViV 


Fig.  76. — Section  through  the  upper  part  of  the  thorax,  viewed  from  below.  The  line 
of  section  is  not  exactly  horizontal,  a  slightly  lower  plane  being  reached  on  the  right  side 
than  on  the  left.  In  order  to  show  the  apical  parietal  pleura,  the  pulmonary  apices  have 
been  removed.  There  can  be  noted  in  this  specimen  the  beginning  contact  of  the  right 
pleura  with  the  trachea,  and  the  anterior  position  of  the  innominate  artery,  whose  bifurca- 
tion is  well  shown.  On  the  left  side,  the  wide  separation  of  the  pleura  from  the  trachea  by 
means  of  the  large  arteries,  esophagus,  and  areolar  tissue  can  readily  be  seen.  The  deep 
position  of  origin  and  the  obliquely  anterior  course  of  the  left  subclavian  artery  is  plainly 
visible.  T,  trachea;  E,  esophagus;  R.A.P.,  right  apical  pleura;  L.A.P.,  left  apical  pleura; 
I. A.,  innominate  artery,  dividing  into  R.S.A.,  right  subclavian  artery  and  R.C.A.,  right 
common  carotid  artery;  L.S.A.,  left  subclavian  artery;  L.C.A.,  left  common  carotid  artery; 
R.S.V.,  right  subclavian  vein;  L.I.V.,  left  innominate  vein. 


If  one  lung  becomes  infiltrated,  its  percussion  note  becomes  higher  in  pitch,  not 
by  virtue  of  any  new  sound  element  added,  but  on  account  of  the  loss  of  the  deeper 
tones.  The  note  of  consolidation  is,  therefore,  to  speak  accurately,  not  actually 
higher  but  relatively  less  low.  It  is  the  prominence  of  the  low-pitched  notes  which 
causes  what  we  know  as  resonance.  The  difference  between  a  resonant  and  a  dull 
note  lies,  however,  not  only  in  the  rate  of  the  vibrations  (pitch)  but  also  to  some  extent 
in  their  amplitude  (intensity).     In  other  words,  the  resonant  note  is  louder  and  carries 


METHODS    AND    RESULTS    OF    PERCUSSION 


85 


further.  For  this  reason  slight  degrees  of  dulness  can  sometimes  be  more  readily 
perceived  at  a  slight  distance  from  the  patient  than  by  the  percussor  himself.  This 
is  due  to  the  fact  that  sound  waves  lose  much  of  their  amplitude  in  transit,  and  the 
difference  between  1  and  0  seems  greater  than  that  between  1  and  2.     Low-pitched 


Fig.  77. — Horizontal  section  of  the  thorax  just  above  the  sternoclavicular  articulation 
viewed  from  beneath.  The  pleura  has  been  dissected  away.  This  photograph  shows  (a) 
the  anterior  position  of  the  innominate  artery,  (b)  the  posterior  position  of  the  left  sub- 
clavian artery,  and  (c)  the  anterior  position  of  the  right  innominate  vein.  R,  first  rib; 
R.I. V.,  right  innominate  vein;  E,  esophagus;  T,  trachea;  I. A.,  innominate  artery;  L.S.V., 
left  subclavian  vein;  L.C.A.,  left  common  carotid  artery;  L.S.A.,  left  subclavian  artery. 

It  also  shows  the  thickness  of  the  dorsal  muscles  through  which  the  percussion  vibrations 
must  penetrate  in  order  to  set  up  vibrations  in  the  lung,  even  above  the  level  of  the  scap- 
ulae. Percussion  must,  therefore,  be  more  forcible  than  on  the  front  of  the  chest.  This 
section,  although  from  a  different  body,  shows  the  same  anatomic  disposition  of  the  large 
vessels  in  relation  to  the  upper  lobes  as  does  Fig.  76.  It  is  in  part  due  to  the  more  anterior 
position  of  the  vessels  in  case  of  the  right  upper  lobe  that  the  percussion  note  on  this  side 
is  normally  less  resonant  than  that  of  its  fellow. 


sounds  having  a  great  vibratory  excursion  carry  further.  In  listening  to  a  distant 
orchestra  we  hear  the  drums  and  bassoons,  not  the  stringed  instruments  or  the  fifes; 
we  hear  the  distant  pounding  of  the  surf,  not  the  swish  of  the  waves.1 

1  Selling:  Deut.  Arch.  f.  kl.  Med.,  vol.  xe. 


86  THE  EXAMINATION  OF  THE  LUNGS 

The  skilled  examiner  can  be  accurate  in  topographic  percussion  within 
a  range  of  from  0.5  to  1.0  cm.  Whichever  method  we  employ,  the  finger 
which  strikes  the  blow  (plexor)  must  fall  vertically,  not  obliquely,  upon 
the  tissues  to  be  percussed  for  thus  greater  penetration  is  ensured.  Fur- 
thermore, it  must  be  quickly  withdrawn,  for  thus  lateral  deviation  and 
radiation  of  vibration  is  minimized,  and  deeper  penetration  ensured. 
In  other  words,  unrhythmic  vibrations  are  produced,  in  contradistinction 
to  rhythmic  ones,  in  which  the  lung  tends  to  vibrate  as  a  whole,  and  in 
which  topographic  delimitation  is  impossible. 

THE  PURPOSE  OF  PERCUSSION 

Percussion  is  practised:  (1)  to  elicit  sound;  (2)  to  determine  resistance. 

Percussion  is  based  upon  the  fact  that  when  the  equilibrium  of  an 
elastic  body  is  briefly  disturbed,  it  is  thrown  into  vibrations,  which  in 
turn  produce  sounds  which  vary  in  intensity,  quality,  duration  and  pitch, 
such  variations  depending  on  the  character  of  the  vibrating  tissue — -the 
amount  of  air  and  the  degree  of  elasticity- — and  on  the  nature  of  the  blow. 

The  bodily  organs  are  of  unhomogeneous  structure  and  for  the  most 
part  not  good  tone  producers,  but  sounds  can  be  produced  in  air-contain- 
ing chambers  and  in  liquid-containing  organs.  The  former  vibrate  more 
easily  and  for  a  longer  time. 

The  vibratory  capacity  of  tissues  depends  upon: 

1.  The  size  and  character  of  the  air-containing  spaces — lungs,  intestines, 
etc. 

2.  The  amount  of  elastic  tissue.  The  skin  and  the  lung  have  a  good 
deal,  the  liver  little.  In  the  lungs  it  is  under  tension,  hence  a  better 
tone  than  that  of  the  skin. 

3.  The  degree  of  tension.  The  greater  the  tension,  the  higher  the  pitch 
— tympanitic  belly.  Human  tissues — the  lung,  intestines,  etc. — vary 
greatly  in  the  degree  of  tension  they  possess.  They  may  be  so  relaxed 
as  to  yield  no  note ;  or  they  may  be  so  tense  as  to  yield  metallic  sounds. 

4.  The  thickness  of  the  tissue.  The  thinner  the  tissue,  the  better  the 
vibration,  the  higher  the  note. 

Various  tissues  vibrate  differently,  and  the  same  tissues  when  altered 
by  disease  in  their  physical  consistencies  yield  an  altered  note.  Percus- 
sion teaches  us  only  physical  differences.  Before  we  can  make  a  diag- 
nosis we  must  add  the  data  obtained  by  inspection,  palpation,  ausculta- 
tion, etc.,  as  well  as  the  knowledge  we  possess  regarding  the  history  and 
symptoms  of  the  patient  and  the  pathology  of  the  disease. 

For  example,  a  dull  note  obtained  over  lung  tissue  teaches  us  that  the 
tissues  are  less  vibratile — contain  less  air — than  is  normally  the  case. 
The  sound  of  the  pleximeter  being  constant,  we  are  justified  in  attribut- 
ing variations  in  the  sound  to  physical  alterations  in  the  underlying 
tissues.  Such  a  dull  note  generally  indicates  consolidation,  but  even  if 
we  are  correct  in  this  assumption  we  have  no  means  of  determining  by 
percussion  with  which  of  the  diverse  types  of  pulmonary  consolidation 
we  are  dealing. 

Percussion  is  also  used  to  outline  the  boundaries  of  organs  when 
neighboring  viscera  possess  different  physical  qualities,  as  for  instance 
the  heart  and  the  lung.  The  most  brilliant  triumphs  of  topographic 
percussion  are  manifested  when  unrhythmic  vibrations  (which  remain 


METHODS  AND  RESULTS  OF  PERCUSSION 


87 


more  or  less  localized)  are  set  up,  and  when  the  tissues  directly  under- 
lying the  point  of  percussion  yield  different  vibrations  than  the  neighbor- 
ing structures,  i.e.,  in  the  normally  distended  healthy  lung.  We  can 
accurately  outline  the  heart  or  the  liver  from  the  lung  since  they  have 
very  different  vibratory  qualities,  but  not  the  liver  from  the  heart,  since 
their  acoustic  properties  are  much  the  same.  Neither  can  we  be  accurate 
in  differentiating  between  the  stomach  and  the  colon,  owing  to  their 


Resonant 


Slight  dulness 


Flat     (absolute 
dulness) 


Tympany 


High-pitched 
tympany 


Fig.  78. — Illustrating  the  different  percussion  sounds  normally  obtained  on  the  right 
anterior  and  the  lateral  aspects  of  the  chest,  as  well  as  the  anatomic  reasons  therefor. 
(Compare  Fig.  88.) 

vibratory  similarity,  nor  can  we  accomplish  much  in  outlining  a  tumor  of 
the  intestine  because  rhythmic  vibrations  (tympanitic  sounds)  are  set 
up,  which  cannot  be  localized. 

The  Sense  of  Resistance. — Hard  and  soft  are  terms  which  we  apply 
to  objects  according  as  their  parts  are  displaceable  with  difficulty  or  with 
ease.  We  derive  our  judgments  from  the  pressure  sense  of  the  skin  and 
the  muscle  sense.  Thus  we  speak  of  a  board-like  resistance,  which  we 
.are  accustomed  to  meet  with  in  massive  consolidations. 

The  attributes  which  give  us  the  impression  of  hardness  or  softness 


88  THE    EXAMINATION    OF   THE    LUNGS 

depend  essentially,  first,  upon  the  elasticity  of  the  percussed  object.  The 
more  elasticity,  the  greater  the  displacement  possible.  Second,  upon  the 
length  of  time  during  which  the  percussed  object  is  out  of  contact.  The 
longer  the  plexor  and  pleximeter  remain  in  contact  the  softer  the  object 
seems  and  vice  versa.  Now  we  noted  under  the  discussion  of  tympany 
that  heavy  and  prolonged  percussion  strokes  were  unfavorable  to  bringing 
out  unrhythmic  vibrations — non-tympanitic  notes.  And  we  find  that  an 
increased  tactile  impression  is  most  common  in  association  with  dulness. 
A  sense  of  increased  resistance  is  not  compatible  with  pure  tympany;  the 
note  which  goes  hand  in  hand  with  such  increased  resistance  is  non-tym- 
panitic, of  slight  intensity,  of  brief  duration,  and  high  in  pitch  (flatness). 
Thus  pulmonary  consolidation  and  more  especially  liquid  exudates,  as  a 
pleural  effusion,  produce  a  marked  increase  in  resistance  which  is  readily 
felt  by  the  underlying  (pleximeter)  finger,  and  which  is  associated  with  a 
short,  high-pitched,  flat  percussion  note. 

Not  infrequently  we  are  able  to  state  positively  whether  a  given  note 
is  either  resonant  or  flat,  even  with  our  ears  closed,  simply  by  our  sense 
of  touch.      Anything  which  diminishes  elasticity  will  increase  resistance. 

THE  TECHNIC  OF  PERCUSSION 

The  patient  may  be  sitting,  standing  or  lying,  the  preference  being  in 
the  order  named.  The  chest  must  be  exposed  or  covered  only  by  an 
examining  cape  (see  p.  21).  Muscular  relaxation  must  be  secured.  A 
revolving  low-backed  chair  or  stool  is  useful,  since  it  renders  change  of 
position  from  front  to  back  easy  and  expeditious. 

The  examiner  proceeds  to  percuss  alternately  corresponding  areas  of 
the  right  and  left  sides  of  the  body  and  to  note  differences  in  the  sound 
and  resistance  encountered.  Many  of  these  differences  are  due  to  normal 
anatomic  causes  and  these  must,  of  course,  be  borne  in  mind. 

Although  it  is  generally  the  custom  to  begin  at  the  top  and  percuss 
to  the  bottom  of  the  chest,  this  method  is,  as  has  been  pointed  out  by 
N.  K.  Wood,  especially  for  beginners,  much  more  difficult,  and  for  the 
following  reasons  more  fraught  with  the  possibility  of  error. 

It  is  much  easier  for  the  ear  to  single  out  a  high  note  from  among 
low  ones,  than  is  the  reverse.  In  tuberculosis  especially,  it  is  the  upper 
part  of  the  lung  which  is  first  and  most  extensively  diseased.  By  begin- 
ning at  the  base,  therefore,  we  are  more  likely  to  have  a  normal  resonance 
and  resistance  to  begin  with.  In  other  words,  it  is  better  to  progress 
from  a  normal  finding  to  pathologic  change,  than  work  from  the  abnormal 
to  the  normal.  This  applies  to  both  the  percussion  sound  and  to  the 
sense  of  resistance. 

Percussion  and  auscultation  of  the  apex  of  the  axilla  will  often  reveal 
physical  signs  which  may  be  sought  in  vain  elsewhere.  This  is  especially 
the  case  in  the  early  stages  of  pneumonia,  in  pulmonary  tuberculosis  and 
in  interlobar  empyema.  The  accompanying  illustration  (Fig.  79) 
depicts  the  position  in  which  the  patient's  arm  should  be  held  for  such 
an  examination.     The  muscles  being  retracted  examination  is  facilitated. 

SPECIAL  VARIETIES  OF  PERCUSSION 

Spinal  Percussion. — Percussion  of  the  spine  while  not  generally  practised,  is  be- 
lieved by  some  physicians  to  have  a  value  in  the  diagnosis  of  deep-seated  aneurisms 
and  tumors,  mediastinal  lymphadenitis,  etc.     There  is  normally  dulness  from  the  first 


METHODS  AND  RESULTS  OF  PERCUSSION 


89 


to  the  fourth  dorsal  vertebrae;  and  "osteal"  note  extends  thence  to  the  last  dorsal  spine; 
the  lumbar  region  yields  an  impaired  note,  and  the  sacral  vertebrae,  tympany.  We 
have  never  been  able  to  convince  ourselves  of  the  value  of  this  method  of  examination 
(see  Fig.  91). 

Threshold  Percussion. — This  is  simply  the  lightest  of  light  percus- 
sion. It  must  be  done  in  an  absolutely  silent  room.  The  pleximeter  is 
laid  lightly  against  the  chest  wall,  only  in  the  interspaces,  the  blow  is 
delivered  upon  the  proximal  end  of  the  second  or  of  the  distal  phalanx 
which  is  bent  at  right  angles  to  its  fellow,  and  in  a  vertical  direction  upon 
the  chest  (orthopercussion).  If  this  is  impossible,  a  stump  of  lead  pencil 
may  be  substituted.  In  other  words,  the  pleximeter  is  not  only  small  but 
vertically  placed.     The  blow  struck  by  the  plexor  is  so  light  that  only 


FlG    79 Position  of  the  patient  while  the  axillary  region  is  being  examined. 

resonant    tissues    produce    any  audible  sound;   when  dull   tissues   are 
struck  their  note  is  below  our  auditory  threshold  (Fig.  80). 

The  Coin  Test.— In  performing  this  test  silver  coins  are  used,  as  the 
plexor  and  pleximeter  respectively.  Percussion  is  practised  over  one 
side  of  the  chest,  auscultation  over  the  opposite  side.  The  object  of 
using  coin  is  to  favor  the  genesis  of  very  unrhythmic  vibrations  (metallic 
sounds).  If  a  pneumothorax  is  present,  the  sounds  heard  through  the 
stethoscope  will  have  a  clear,  vibrant,  bell-like  quality,  owing  to  the 
resonating  quality  of  a  large  cavity.     In  such  a  case,  the  com  test  is  said 


90 


THE    EXAMINATION    OP    THE    LUNGS 


to  be  present  and  the  presence  of  pneumothorax  is  practically  established. 
Normal  lung,  solidified  lung  and  simple  effusions  yield  only  a  dull,  short 
metallic  note  closely  similar  to  that  heard  over  the  healthy  lung  (see 
Fig.  60). 

Auscultatory  Percussion. — This  is  occasionally  of  use  in  outlining 
organs.  The  bell  of  the  stethoscope  is  placed  over,  let  us  say,  the  heart. 
It  is  held  in  position  by  the  patient  or  an  assistant  while  the  examiner 
percusses  lightly  the  surrounding  regions  in  a  circular  direction. 


Fig.  80. — Orthopercussion.  Generally  employed  in  conjunction  with  a  very  light  per- 
cussion stroke.  The  pleximeter  surface  being  small  and  the  blow  vertical,  great  accuracy 
may  be  obtained.  This  method  is  especially  recommended  for  outlining  the  left  border  of 
the  heart. 

We  begin  at  a  distance  from  the  heart  and  percuss  toward  it  in  a 
series  of  circles.  The  tissues,  the  sound  of  which  is  to  be  compared,  must 
be  equally  distant  from  the  stethoscope,  as  under  normal  conditions 
the  sound  will  increase  in  intensity  in  approaching  the  point  ausculted. 
As  soon  as  the  organ  is  reached  by  the  percussion  blow  the  sound  will 
greatly  increase  in  intensity  and  we  know  that  its  outer  boundary  has 
been  reached.  Instead  of  percussing  some  examiners  use  a  vibrating 
tuning  fork,  placing  the  butt  of  the  same  against  the  chest  wall  in  order 
to  set  up  intrathoracic  vibrations. 


CONDITIONS  MODIFYING  PERCUSSION  SOUNDS 

1.  Any  thickening  of  the  superficial  tissues  tends  to  diminish  pene- 
tration of  the  percussion  blow  and  to  deaden  sound.  The  commonest 
causes  are:  adiposity,  large  muscles,  or  mammary  glands  and  edema. 

2.  When  the  bony  thorax  is  large  and  deep,  we  have  a  more  powerful 


METHODS    AND    RESULTS    OF    PERCUSSION  91 


Fig.  81. — Auscultatory  percussion. 


Fig.  82. — Auscultatory  percussion.     The  hell  of  the  stethoscope  is  placed  at  B]>nd  per- 
cussion is  performed  in  gradually  narrowing  circles  toward  the  heart. 


92 


THE    EXAMINATION    OF    THE    LUNGS 


resonator.  This  tends  to  cause  a  note  of  lower  pitch.  When  the  costal 
cartilages  are  ossified,  the  thorax  becomes  more  rigid,  and  less  penetra- 
tion of  the  percussion  blow  occurs  because  a  greater  portion  of  the  impact 
is  transferred  laterally  by  the  arch-like  structure  of  the  ribs,  accurate 
topographic  percussion  is,  therefore,  more  difficult. 

3.  Thickening  of  the  pleura,  or  exudation  or  effusion  into  the  pleural 
cavity  cause  both  a  diminished  penetration  of  the  percussion  blow  and  a 
lessened  resonance  of  sound,  because  the  vibrations  lose  much  of  their 
amplitude  in  passing  through  media  of  different  density. 

4.  Changes  in  the  pulmonary  tissue — the  degree  of  tension,  the  amount 
of  air,  elasticity  and  density — produce  marked  and  important  alterations 
of  sound. 


Fig.  83. 


Fig.  84. 


Figs.  83  and  84. — Showing  the  areas  over  which  the  percussion  note  is  shorter,  higher 
pitched  and  less  resonant  than  normal  in  dextro-convex  scoliosis.  These  changes  are  most 
marked  over  the  area  I,  and  least  marked  over  the  area  IV.  (After  E.  A.  Gray,  Jour.  Am. 
Med.  Assn.,  1912,  LIX,  2249.)     (See  Figs.  17,  34,  36.) 


I.  Changes  in  pulmonary  tension  may  be  uni-  or  bilateral. 

(a)  Increased  tension  occurs  during  forced  inspiration  and  in  emphy- 
sema.    This  causes  more  rapid  vibrations  and  a  higher-pitched  note. 

(b)  Decreased  tension. 

(1)  General,  may  arise  from  pleural  effusions,  increased  intra-ab- 
dominal pressure  (ascites,  tumors) ;  it  also  occurs  in  senility  (less  elastic 
and  more  rigid  thorax).  Decreased  tension  allows  the  lung  to  vibrate 
as  a  whole.  This  adds  a  tympanitic  quality  to  the  percussion  note. 
The  high-pitched  tympany  which  occurs  above  pleural  effusions  and 
around  consolidations  is  known  as  Skodaic  tympany. 

(2)  Local  decrease  of  tension  occurs  around  consolidated  areas 
(pneumonia,  tuberculosis,  etc.). 

II.  Changes  in  the  Amount  of  Air  in  Lung  Tissue. — (a)  An  increase 
occurs  in  emphysema,  asthma  and  during  compensatory  (forced)  breath- 
ing, also  in  cases  of  cavitation.     In  the  first  case  the  percussion  note 


METHODS    AND    RESULTS    OF    PERCUSSION  93 

is  hyperresonant,  in  the  last,  tympanitic,  provided  that  the  cavity  is 
sufficiently  large,  not  too  deeply  placed,  and  that  it  is  filled  with  air. 
In  the  first  instance  the  vibrating  tissues  are  thinner  under  greater  ten- 
sion and  contain  more  air.  In  the  latter  the  walls  of  the  cavity  vibrate 
in  unison  with  the  air  columns  it  contains.  During  forced  inspiration 
deep  percussion  yields  a  lower;  light  percussion,  a  higher  note,  than 
during  forced  expiration. 

(b)  Decreased  air  bearing  lung  tissue  occurs  in  consolidation  (pneu- 
monia, tuberculosis,  fibrosis,  atelectasis  with  compression,  cavities 
filled  with  exudate,  etc.).  The  percussion  note  becomes  less  resonant 
in  proportion  to  the  consolidation,  because  the  vibrating  tissues  are 
thicker,  less  elastic  and  contain  less  air.  The  sound,  therefore,  becomes 
short,  high-pitched  and  dull,  and  resistance  is  increased. 

Even  minor  degrees  of  spinal  curvature  may  produce  lack  of  resonance 
over  certain  areas  of  the  chest.  This  is  due  to  the  fact  that  abnormal 
convexities  of  the  thorax  produce  an  increased  rigidity  of  the  more  con- 
vex rib  which  tends  to  prevent  penetration  of  the  percussion  blow,  whereas 
a  flattened  rib  has  the  opposite  effect  (Sahli)  (Figs.  17,  26,  36,  83,  84). 

In  order  to  detect  spinal  deformities  the  patient  should  be  sitting, 
muscularly  relaxed,  and  the  examiner  should  note  especially:  the  relative 
height  of  the  shoulders  and  of  the  scapulas,  the  depth  of  the  supra- 
clavicular fossa?,  and  in  women  the  height  of  the  breasts.  The  spine 
itself  is,  of  course,  also  inspected  both  from  a  lateral  and  from  an  antero- 
posterior aspect.  Small  degrees  of  scoliosis  may  be  emphasized  by  mark- 
ing the  skin  over  the  spinous  processes  of  the  vertebras  with  a  pencil. 


CHAPTER  VII 

NORMAL  VARIATIONS  OF  THE  PULMONARY  PERCUSSION 

SOUNDS 

INDIVIDUAL  VARIATIONS 

There  is  no  invariable  normal  standard.  Actual  values  must  be 
determined  largely  by  the  variation  of  the  two  sides  of  the  chest,  but 
the  normal  range  must  be  learned  by  experience.  Percussion  sounds 
will  vary  with:  (a)  the  soft  parts  overlying  the  lungs;  (b)  the  flexibility 
of  the  thorax;  (c)  the  size  and  shape  of  the  lungs,  and  their  state  of 
tension;  (d)  the  region  percussed. 


Fig.  85. — Showing  normal  areas  of  dulness  and  flatness  caused  by,  and  outlining  the 
anatomic  position  of,  the  heart  and  the  liver.  The  lower  border  of  the  heart  cannot  be  out- 
lined since  it  overlies  the  liver  and  these  organs  have  acoustically,  in  so  far  as  percussion  is 
concerned,  identical  qualities.  The  heavy  shading  indicates  the  part  of  these  organs  which 
are  uncovered  by  lung  tissue  and  therefore  yield  a  flat  note.  The  arrows  indicate  the  di- 
rection in  which  percussion  should  proceed.  The  light  shading  shows  the  areas  over  which 
clear  pulmonary  resonance  is  replaced  by  slight  dulness  owing  to  the  proximity  of  the  under- 
lying liver  and  heart.     (See  Figs.  86,  167.) 

REGIONAL  VARIATIONS 

Anteriorly. — The  clearest  pulmonary  resonance  is  encountered  below 
the  clavicles  and  at  the  angles  of  the  scapulae.  In  women  a  diminution 
of  resonance  and  an  elevation  of  pitch — owing  to  the  mamnice — begins 
below  the  second  interspace.  On  the  left  side  cardiac  dulness  begins  at 
the  upper  border  of  the  third  rib,  and  on  the  right,  the  hepatic  dulness, 
below  the  fourth  interspace.  The  note  on  approaching  these  organs 
becomes  progressively  less  resonant  until  absolute  flatness  is  encountered 

94 


VARIATIONS    OF    PULMONARY    PERCUSSION    SOUNDS 


95 


— no  lung  tissue  intervening  between  the  organ  and  the  chest  wall. 
Diminished  resonance  is  also  encountered  in  the  splenic  region,  but  the 
spleen  cannot  be  accurately  outlined  by  percussion  (Fig.  87).  There  is 
less  resonance  at  the  sterno-clavicular,  than  at  the  sterno-acromial  angle, 
and  less  resonance  over  the  second  rib  than  over  the  second  interspace. 
Over  the  upper  sternum  the  osteal  quality  predominates,  below  the  second 
rib  more  pulmonary  resonance  may  be  elicited,  especially  on  light 
percussion. 

Shortly  before  the  lower  costal  margin  is  reached  the  note  becomes 
slightly  tympanitic   owing  to  the  underlying  air-containing  viscera— 


Fig.  86. — Window  dissection  of  the  chest  from  in  front,  showing  the  position  of  the  heart 
and  liver  which  causes  the  dull  areas  charted  in  Fig.  85.  The  pericardium  has  been  re- 
moved. The  area  of  absolute  (superficial)  cardiac  dulness  is  larger  than  normal,  because 
the  lungs  were  frozen  in  the  position  of  expiration.  The  amount  of  heart  exposed  is  there- 
fore unusually  large.  Not  infrequently  the  anterior  pulmonary  margins  overlap  in  front, 
leaving  very  little  of  the  heart  exposed.     (See  Fig.  85.) 

stomach  and  intestines  (Fig.  78).  On  this  account  liver  dulness,  espe- 
cially to  the  right  of  the  right  para-sternal  line,  often  does  not  extend 
to  quite  the  lower  margin  of  the  ribs  unless  the  organ  is  enlarged. 

On  the  left  side  near  the  lower  costal  margin  a  tympanitic  area — 
Traube's  semilunar  space — is  encountered.  The  tympany  is  caused  by 
that  area  of  the  stomach  which  lies  between  the  left  lower  margin  of  the 
lung,  the  right  border  of  the  spleen  and  the  right  border  of  the  liver. 
It  disappears  when  the  stomach  is  filled  with  food  and  in  cases  of  peri- 
cardial effusion.     It  is  diagnostically  of  little  importance  (Fig.  89). 

Dulness  over  the  left  lateral  pulmonary  margin  may  be  caused  by  a 


96  THE    EXAMINATION    OF    THE    LUNGS 

full  stomach,  and  tympany  in  this  region  is  often  due  to  gaseous  disten- 
tion. These  facts  must  be  borne  in  mind  or  diagnostic  errors  will  be 
made  (Fig.  90). 

Posteriorly. — The  supraspinous  fossae  despite  the  thickness  of  the 
overlying  muscles,  gives  a  certain  amount  of  pulmonary  resonance, 
especially  in  women  and  in  emaciated  individuals  (Figs.  76,  77,  91). 
The  upper  scapular  region  is  less  resonant  than  the  lower,  especially 


Fig.  S7. — Splenic  dulness.  Percussion  of  the  spleen  has  but  little  value  unless  the 
organ  is  enlarged,  and  when  this  is  the  case  palpation  is  a  more  satisfactory  method  of 
examination.     (Compare  Figs.  61  and  70.) 

over  the  spine.  The  interscapular  region  lies  between  the  range  of  these 
two.  The  infrascapular  region  gives  a  clear  resonance  on  light  percus- 
sion as  far  downward  as  the  eleventh  interspace,  but  forcible  percussion 
brings  out  the  dulling  due  to  the  liver,  as  high  as  the  ninth  or  even  the 
eighth  rib  on  the  right  side.  On  the  left  side  the  note  is  variably  modified 
by  the  neighboring  influence  of  the  stomach  and  spleen  (Fig.  61).  In  the 
axillary  region  hyperresonance  is  often  encountered;  in  the  lower  por- 
tions, the  stomach  imparts  a  tympanitic,  and  the  liver  a  dull  quality  as  we 
approach  the  level  of  the  diaphragm. 


VARIATIONS    OF    PULMONARY    PERCUSSION    SOUNDS 


97 


The  percussion  outlines  of  the  lung  vary  with  the  phase  of  respiration. 
One  can  map  out  the  superior,  inferior,  and  precordial  margins.  Respira- 
tion changes  the  percussion  note,  by  altering  the  volume,  tension  and 
density  of  the  pulmonary  tissue  and  by  displacing  organs. 

The  superior  margin  of  the  lung  extends  2  to  3  cm.  (1V±  inches) 
above  the  clavicles  at  the  end  of  a  quiet  respiration. 

There  has  been  much  discussion  as  to  whether,  and  to  what  extent  the  apices  move 
during  respiration.  It  seems  definitely  established  that  only  the  anterior  and  lateral 
aspects  can  move  and  that  there  is  a  slight  upward  movement  during  inspiration. 
Over  the  anterior  slope  of  the  apex  lies  a  lid  consisting  of  fibrous  fascia,  the  first  rib, 


Pleura    5th  rib    Int.  mammary  artery- 


Liver 


Lung 


Descending  aorta        Inf.  vena  caya 


Fig.  88. — Transverse  section  through  the  thorax  from  the  lowest  part  of  the  ensi- 
form  cartilage  to  the  bottom  of  the  ninth  dorsal  vertebra.  The  following  points  are  to  be 
noted: 

1.  Liver  dulness  is  demonstrable  by  percussion  on  the  right  side  of  the  chest  only;  on  the  left  side 
this  organ  is  too  deeply  placed.     (Compare  Fig.  78.) 

2.  The  liver  extends  even  further  to  the  left  than  does  the  heart  which  rests  upon  it,  only  the  dia- 
phragm separating  these  two  structures.  In  case  of  abdominal  distention  (ascites,  meteorism)  the  dia- 
phragm encroaches  even  more  upon  the  pleural  cavity  than  in  the  normal  case  here  shown.  For  this 
reason  the  pulmonary  bases  may  yield  a  dull  note  on  percussion  in  cases  of  ascites,  even  in  the  erect 
position  .and- in  the  absence  of  pulmonary  congestion  or  hydrothorax  (upward  displacement  of  the 
liver) . 

3.  This  section  passes  through  the  heart  2  cm.  above  its  lowest  level,  the  pericardium  which  con- 
tained half  an  ounce  of  serous  fluid  extended  2  cm.  below  the  level  of  the  heart.  In  the  performance 
of  paracentesis  pericardii  there  is  less  danger  of  puncturing  the  pleura  if  the  trochar  is  introduced  in  the 
fifth  interspace  on  the  left,  close  to  the  sternum.  At  this  point  both  the  pleura  and  the  internal 
mammary  vessels  will  be  avoided.     (Figure  redrawn  after  Braune.) 


the  subclavian  artery  and  vein.  This  lid  is  hinged  from  behind.  When  its  anterior 
part  is  lifted  up  during  inspiration,  it  is  the  anterior  part  of  the  apex  which  feels  the 
movement;  the  posterior  portion  lying  in  front  of  the  neck  of  the  first  rib,  being  nearer 
the  axis,  is  affected  only  indirectly  (Fig.  93)  (Keith,  Journal  of  Anatomy  and  Physi- 
ology, May,  1903.     Appendix,  Proc.  Anat.  Soc.  Gr.  Brit.  &  Ireland,  May,  1903). 

Percussion  of  the  Supraclavicular  Fossa. — The  idea  that  a  failure  of  the 
percussion  resonance  to  move  upward  during  forced  inspiration  indicates 
apical  adhesions  or  infiltration  is  erroneous.  Such  an  increase  in  reson- 
ance is  not  always  present  under  normal  conditions,   and   when  so,  is 

7 


98 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.  89. — Traube's  semilunar  space. 


Fig.  90. — Dulness  due  to  a  full  stomach. 


VARIATIONS    OF    PULMONARY    PERCUSSION    SOUNDS  99 

mainly  an  indication  that  the  apex  of  the  lung  has  become  broader, 
deeper.  As  has  been  stated  above,  there  is  practically  no  upward  move- 
ment. Since  the  clavicles  move  with  respiration,  they  cannot  be  taken 
as  accurate  fixed  points,  from  which  to  judge  of  apical  expansion. 

The  Inferior  Pulmonary  Margin. — During  forced,  held  inspiration,  the  percussion 
note  becomes  slightly  higher-pitched,  because  of  the  increased  tension  of  the  pul- 
monary tissue.     The  lower  border  of  the  pulmonary  resonance  should  be  noted  during 


Fig.  91. — Window  dissection  of  the  back,  showing:  1.  Thickness  of  dorsal  muscles  through 
which  the  percussion  vibrations  must  penetrate  before  reaching  the  pulmonary  tissue.  2. 
The  bronchial  bifurcation  over  which  area  the  breath  sounds  are  normally  broncho-vesicular, 
the  fremitus  and  vocal  resonance  intense.  A,  aorta;  B,  bronchial  bifurcation;  L.A.,  left 
auricle;  T.A.,  thoracic  aorta;  E,  esophagus.  Forcible,  two-finger  percussion  is  sometimes 
necessary  to  elicit  pulmonary  resonance  at  the  level  of  the  shoulder  girdle.  3.  This  dissec- 
tion further  illustrates  the  reason  why  spinal  percussion  has  practically  no  value.  The 
distance  of  the  mediastinal  viscera  from  the  point  percussed  and  the  thickness  of  the  spinal 
column  render  the  penetration  of  percussion  vibrations  well-nigh  impossible. 

quiet  breathing  and  its  distance  from  the  level  of  the  seventh  cervical  vertebra  noted. 
The  patient  is  then  asked  to  take  as  deep  an  inspiration  as  possible  and  hold  it.  The 
line  of  pulmonary  resonance  will  move  downward  several  centimeters  during  this 
procedure.  The  absence  of  this  phenomenon  may  be  due  to  pleural  adhesions  or 
effusion,  pulmonary  fibrosis  or  infiltration  (see  Fig.  50). 

During  quiet  respiration  the  margins  of  the  lungs  move  but  little.  In  the  dorsal 
position,  the  anterior  margin  moves  downward  about  2  cm.  (%  inch)  lower  than  in 
the  erect  posture.     In  lateral  decubitus  the  edge  of  the  lung  on  the  upper  side  moves 


100 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.  92. — Oblique  view  of  the  mediastinal  viscera  from  the  right  posteriorly,  showing 
A,  aortic  arch;  A',  thoracic  aorta  (reflected);  R,  recurrent  laryngeal  nerve;  L.A.,  left 
auricle;  L.V.,  left  ventricle;  L.P.A.,  left  pulmonary  artery;  L.S.V.P.,  left  superior  pul- 
monary vein;  L.I.P.V.,  left  inferior  pulmonary  vein;  E,  esophagus  (reflected).  The  left 
recurrent  laryngeal  nerve  is  not  infrequently  compressed  in  aneurisms  of  the  arch  of  the 
aorta.  This  results  in  a  localized  neuritis  which  is  clinically  manifested  by  a  husky  voice,  a 
"brassy"  cough  and  sometimes  "rattling  in  the  throat."  The  nerve  may  be  compressed 
indirectly  in  some  cases  of  mitral  stenosis.  *  The  right  auricle  being  greatly  dilated  presses 
the  left  pulmonary  artery  upward,  squeezing  the  nerve  between  this  vessel  and  the  aortic 
arch. 

*  Fetterolf,  G.  and  Noeris,  G.  W.:  "The  Anatomic  Explanation  of  the  Paralysis  of  the  Left  Re- 
current Laryngeal  Nerve  Found  in  Certain  Cases  of  Mitral  Stenosis."     Am.  Jour.  Med.  Sc,  May,  1911. 


VARIATIONS    OF    PULMONARY    PERCUSSION    SOUNDS  101 

down  3  to  4  cm.  During  forced  breathing  the  excursion  may  amount  to  9  cm.  (3J^ 
inches). 

Respiratory  displacement  of  the  lung — which  occurs  through  a  filling  of  the  com- 
plemental  space — is  most  marked  in  the  axillary  line.  The  lower  pulmonary  border 
never  descends  nearer  to  the  lower  costal  margin  than  7  cm.  (2%  inches)  on  the  right, 
and  5  cm.  (1.96  inches)  on  the  left  side  (see  Figs.  9,  10,  11). 

Pathologic  Displacement. — Downward  displacement  of  the  lower  lung  border  may 
be  permanent  (emphysema)  or  temporary  (asthma).  Upward  displacement  of  the 
lower  pulmonary  border  occurs  in  cases  of  pleural  or  pulmonary  contraction  fibrosis), 
and  in  intraperitoneal  enlargement. 


ms/)  it. 


Fig.   93. — A  figure  to  show  the  relationship  of  the  first  rib  and  manubrium  sterni  to  the 
apex  of  the  lung  (1)  in  expiration,  (2)  in  inspiration.     (Keith.)      (See  p.  97.) 


OTHER  VARIATIONS 

Sex. — In  women  the  upper  chest  is  more  resonant  as  compared  to 
the  lower,  than  in  men,  clue  to  the  habit  of  upper  thoracic  breathing. 
The  mammary  region  is  often  difficult  to  percuss  on  account  of  the  thick- 
ness of  the  tissues. 

Age. — In  old  age  the  costal  cartilages  become  ossified,  resulting  some- 
times in  a  higher-pitched,  less  resonant  note.  In  other  cases  a  more 
tympanitic  quality  is  heard.  These  alterations  are  in  part  due  to  tho- 
racic rigidity,  and  in  part  to  the  condition  of  the  lungs,  depending  upon 
whether  senile  pulmonary  atrophy,  or  emphysema  has  occurred.  The 
rigid  thorax  tends  to  prevent  deep  penetration  of  the  percussion  blow. 

THE  DIAPHRAGM 

The  position  of  the  diaphragm  may  be  determined  by:  (a)  percussing 
the  lower  border  of  the  lungs ;  (b)  percussing  the  upper  border  of  the  liver 
and  spleen;  (c)  observing  Litten's  phenomenon;  (d)  Harrison's  groove 
if  present;  and  (e)  by  means  of  the  X-ray. 

The  lungs  do  not  fill  the  pleural  sac  during  quiet  respiration,  but  leave  a  semi- 
circular space — the  complimental  space  of  Gerhardt,  between  the  chesl  wall  and  the 
shelving  diaphragm.  The  right  phrenic  dome  is,  as  a  rule,  1  inch  higher  than  the  left , 
but  both  may  be  equal  or  the  normal  difference  even  reversed  (see  Fig.  59).  During 
inspiration  a  recession  downward  is  noted,  but  hardly  any  appreciable  flattening, 
except  with  forced  inspiration.  The  extent  of  the  excursion  in  quiet  breathing  is 
%  inch;  in  forced  respiration  2%  to  5  inches.  The  diaphragm  is  normally  lowest 
while  sitting,  intermediate  in  standing  (active  abdominal  muscles)  and  highesl  in 
recumbency.  In  the  right  lateral  decubitus,  the  right  dome  is  higher  (greater  weight 
of  the  abdominal  contents),  and  vice  versa,  notwithstanding  this  fact   the  excursion  is 


102  THE    EXAMINATION    OF    THE    LUNGS 

greater  on  the  dependent  side  (muscles  act  more  forcibly  against  resistance),  the  upper 
side  remains  relatively  motionless  (decreased  excursion  because  of  approximation 
of  the  diaphragmatic  origin  and  insertion). 

Alterations  in  arching  and  mobility  are  almost  a  constant  factor  in  pulmonary  tuber- 
culosis, especially  if  there  is  fibrosis  or  basal  pleural  adhesions.  In  unilateral  cases, 
the  fluoroscope,  generally  show  a  high,  well-arched  dome  on  the  affected  side  which 
moves  only  slightly,  and  a  low  flattened  dome  on  the  sound  side  (compensatory 
emphysema). 

SOME  PHYSIOLOGIC  CONSIDERATIONS 

The  diaphragm  is  the  chief  means  of  inspiration.  In  quiet  breathing 
the  main  function  of  the  intercostals  is  to  fix  the  ribs,  and  maintain  expan- 
sion during  the  descent  of  the  diaphragm.  When  the  latter  is  hindered 
or  inspiration  becomes  labored  the  intercostals  act  more  strongly,  so  as 
to  raise  the  ribs  and  dilate  the  thorax.  In  very  forcible  inspiration  other 
muscles  act  also:  sternomastoid,  scaleni.  omohyoids,  upper  part  of  the 
trapezii.     These  muscles  hypertrophy  from  overuse— emphysema. 

Elevation  of  the  ribs  is  also  in  part  produced  by  the  diaphragm 
(normal  position  is  one  of  arched  tension)  which  acts  by  contracting 
over  the  liver  and  the  abdominal  viscera  as  a  fulcrum.  The  latter  are 
pressed  upward  by  the  abdominal  muscles.  If  "the  ribs  remain  fixed 
the  diaphragm  cannot  be  pushed  upward,  but  if  the  abdominal  muscles 
pull  the  ribs  inward,  then  the  tension  of  the  diaphragm  is  relaxed  and 
the  abdominal  viscera  under  the  pressure  of  the  abdominal  muscles, 
can  drive  it  upward  and  expel  the  supplemented  air"  (Hutchison). 
The  diaphragm  and  intercostals  are  antagonists  although  they  concur 
to  produce  the  same  result.  The  liver  and  the  intercostal  muscles  pre- 
vent the  diaphragm  from  drawing  the  chest  in. 

Forced  inspiration  exerts  its  effects  mainly  upon  the  upper  chest  and 
the  true  ribs. 

Quiet  expiration  is  due  not  merely  to  cessation  of  muscular  contrac- 
tion— a  passive  act,  the  result  of  elastic  recoil — but  also  to  active  relaxa- 
tion (of  the  inspiratory  muscles).  The  muscular  effort  required  by  an 
inspiration  is  equivalent  to  raising  100  pounds;  a  forced  inspiration  to 
raising  300   pounds    (Hutchison). 

Forced  expiration  is  due  to  the  activity  of  the  abdominal  muscles, 
the  latissimi  dorsi,  and  lower  part  of  the  trapezii.  It  exerts  its  effect 
mainly  upon  the  lower  chest  and  false  ribs. 

Paralysis  of  the  diaphragm  causes  bilateral  enlargement  of  the  chest. 
Paralysis  of  the  intercostal  muscles,  bilateral  diminution  in  size. 

Respiratory  pressure  changes  are  most  marked  in  the  lower  part  of 
the  pleural  sac,  and  least  marked  between  the  tracheal  bifurcation  and 
the  heart  (Meltzer  and  Auer). 

During  inspiration  the  interspaces  are  pushed  inward  by  the  atmos- 
pheric pressure.     This  is  most  evident  in  the  lower  interspaces. 

The  visceral  pleura  is  retained  in  contact  with  the  parietal  pleura  by 
an  "atmospheric  ligament"  (Keith)  due  to  the  atmospheric  pressure 
(15  pounds  to  the  square  inch),  by  way  of  the  bronchii  exerting  its  force 
against  the  negative  intrathoracic  pressure.  "  The  weight  required  to 
separate  the  visceral  from  the  parietal  pleura  over  both  lungs  amounts 
to  about  a  ton"  (Hutchison),  a  far  greater  force  than  can  be  brought 
to  bear  by  the  respiratory  muscles,  hence  the  two  pleural  membranes 
remain  in  contact.     But  if  one  lung  collapses  from  a  pneumothorax  or 


VARIATIONS    OF    PULMONARY    PERCUSSION    SOUNDS  103 

pleural  effusion,  it  is  dragged  toward  the  opposite  side  by  its  fellow 
even  before  the  presence  of  an  exudate  causes  displacement  by  means 
of  actual  pressure.  The  negative  pressure  exerted  by  the  lungs  upon  the 
pleura  favors  exudation  (hydrothorax)  when  the  vascular  engorgement 
of  the  pleura  exists.  Very  considerable  exudation  must  occur  before 
the  pressure  becomes  positive.  This  fact  is  a  strong  argument  in  favor 
of  the  early  aspiration  of  pleural  effusions.     The  greater  the  elasticity 


Fig.  94. — Diagram  illustrating  the  direction  of  the  ''pull"  of  the  lungs  which  is 
due  to  their  elasticity  and  which  occurs  when  they  are  relaxed  as  in  pneumothorax. 
(After  Hutchison.) 

or  tonus  of  the  lung,  the  greater  will  be  its  traction  when  the  opposing 
lung  is  collapsed.  Hence  pneumothorax  occurring  with  relatively  healthy 
lungs,  free  from  pleural  adhesions,  will  cause  greater  mediastinal  displace- 
ment and  shock,  than  if  the  lungs  have  partially  lost  their  elasticity  or 
are  bound  fast  by  adhesions  (Hutchison)  (see  p.  575). 

The  negative  intrathoracic  pressure  is  about  as  follows: 

Mg.    Hg. 

Normal  inspiration - —   10 

Normal  expiration —      7 

Deep  inspiration —   40 

Deep  expiration —     0 

Deep  inspiration  with  air  passages  closed — 100 

Deep  expiration  with  air  passages  closed +100 


CHAPTER  VIII 

AUSCULTATION 

Auscultation,  the  discovery  of  which  we  owe  to  Laennee,  is  the  act 
of  listening  for  sounds  produced  within  the  body,  chiefly  those  of  the 
heart  and  the  lung. 

I.  Immediate  or  direct  auscultation  is  performed  by  placing  the  ear 
against  the  chest  wall.  This  method  is  still  much  used  for  listening  to 
the  sounds  produced  in  the  lung.  By  its  employment  we  get  more  bone, 
than  air  conduction.  The  sounds  heard  are  generally  less  loud  and  clear 
than  those  heard  through  the  stethoscope,  and  accurate  localization  is 
not  as  readily  possible.  If,  and  tins  should  but  rarely  happen,  the  ex- 
amination must  be  made  through  garments,  the  unaided  ear  is  preferable 
to  the  stethoscope.  Vocal  resonance  may  sometimes  be  better  appreciated 
by  the  immediate  method. 

II.  Mediate  or  indirect  auscultation  is  practised  by  interposing  some 
sound  conducting  material — a  stethoscope — between  the  ear  and  the 
body.  This  method  is  now  generally  employed,  especially  in  auseulting 
the  heart.  It  has  the  following  advantages.  The  examiner  can  localize 
sound  more  sharply,  he  can  assume  a  more  comfortable  position,  he  comes 
into  less  intimate  contact  with  the  patient,  he  can  auscult  certain  regions 
such  as  the  supraclavicular  fossae,  and  the  axillary  apices  which  would 
otherwise  remain  inaccessible. 

THE  METHOD 

It  is  essential  that  both  patient  and  examiner  be  in  as  comfortable 
a  position  as  possible.  The  former  will  then  relax  his  muscles  and  breathe 
more  regularly,  the  latter  will  be  better  able  to  concentrate  his  entire 
attention  upon  what  he  hears.  The  sitting  posture  should  be  chosen  when 
possible. 

For  a  satisfactory  examination  it  is  essential  that  the  part  to  be 
ausculted  be  bared  to  the  skin.  After  having  been  put  both  mentally 
and  physically  at  ease,  the  patient  should  be  told  to  breathe  a  trifle  more 
deeply  than  is  normally  the  case,  with  the  mouth  open.  All  raucous, 
throaty  sounds  or  voluntary  expiration  must  be  avoided  since  they 
vitiate  the  results  of  the  examination.  It  is  a  waste  of  time  to  attempt 
auscultation  of  the  lungs  until  the  patient  breathes  properly.  A  begin- 
ning may  be  made  at  the  top  or  bottom  of  the  chest  and  the  stethoscope 
gradually  moved  from  one  interspace  to  another  until  the  entire  chest 
has  been  ausculted;  at  each  step  comparing  the  sounds  of  a  similar  area 
on  the  opposite  side  of  the  chest,  in  the  anterior,  lateral  and  posterior 
regions.     The  supraclavicular  fossae  must  not  be  overlooked. 

The  bell  of  the  stethoscope  is  placed  firmly  against  the  skin  so  as  to 
exclude  external  sounds,  but  too  great  pressure  is  to  be  avoided,  since 
it  increases  skin  tension,  diminishes  elasticity  and  deadens  sound.     Con- 

104 


AUSCULTATION 


105 


siderable  pressure  may  occasionally  be  necessary  in  order  to  bring  the 
bell  nearer  to  the  source  of  the  sound,  as  in  the  case  of  ausculting  the 
fetal  heart  sounds,  also  at  times  to  elicit  pleural  or  pericardial  friction 
sounds  by  bringing  the  inflamed  serous  surfaces  into  more  intimate 
contact. 

Auscultation  is  sometimes  rendered  difficult  by  the  presence  of 
cutaneous  hair,  edema  or  emphysema.  In  the  first  instance  the  crackling 
of  the  hair  may  be  obviated  by  shaving  or  by  simply  wetting  the  hair. 


L.C.A.  L.S.A.A. 


iiaL^f-a  •  .5   l.m.a 


R.V.N. 

E. 


D.A. 


Fig.  95. — Broncho-vesicular  breath  sounds  are  often  due  to  stenosis  of  the  upper  air 
passages.  If  the  patient's  neck  is  sharply  turned  toward  either  side,  if  he  has  hypertrophied 
tonsils,  adenoids,  etc.,  such  sounds  may  be  produced  in  normal  lungs.  They  are  to  be  differ- 
entiated from  pathologic  sounds  by  the  fact  that  the  harshness  is  bilateral,  is  often  audible 
at  a  distance  when  the  patient  breathes  deeply,  that  they  may  be  greatly  modified  by  open- 
ing the  mouth,  and  by  the  fact  that  they  are  unassociated  with  other  physical  signs  in- 
dicative of  pulmonary  consolidation. 

The  illustration  shows  a  stenotic  trachea  due  to  enlargement  of  the  thyroid  gland. 
Also  the  intimate  contact  of  the  right  pulmonary  apex  with  the  trachea,  in  contrast  to  the 
marked  separation  of  these  structures  on  the  left  side.  A,  aorta;  D.A.,  descending  aorta; 
R.S.A.,  right  subclavian  artery;  R.C.A.,  right  carotid  artery;  L.S.A.,  left  subclavian  artery; 
L.C.A.,  left  carotid  artery  ;L.M.  A.,  left  mammary  artery;  E,  esophagus;  R.V.N. ,  right  vagus 
nerve. 


Extraneous  Sounds,  Etc. — Practice  enables  us  to  concentrate  our 
attention  on  a  particular  element  of  a  complex  sound  and  to  disregard 
the  rest.  Thus  when  we  listen  to  the  heart  we  ignore  the  perfect  In- 
audible respiratory  sounds  and  vice  versa.  Furthermore,  certain  other 
noises  must  be  prevented  or  equally  eliminated  from  our  consciousness, 
e.g.:  (a)  noises  in  the  room;  (6)  sounds  produced  by  friction  of  the  stetho- 
scope against  the  examiner's  finger  or  patient's  skin  during  the  act  of 
breathing  or  by  the  rhythmic  encroachment  of  a  neighboring  rib,  or 


106  THE    EXAMINATION    OF   THE    LUNGS 

by  the  fact  that  some  part  of  the  rubber  tubing  comes  into  contact  with 
the  garments,  etc.;  (c)  sounds  produced  by  the  interposition  of  garments 
between  the  ear  and  the  chest.  Needless  to  say  it  is  useless  to  attempt 
to  auscult  through  stiff  materials  such  as  starched  linen,  (d)  Contract- 
ing muscle  produces  a  sound,  hence  any  muscular  tremor  or  voluntary 
stiffening  of  muscles  on  the  part  of  the  patient  must  be  prevented.  The 
examining  room  must  not  be  cool  enough  to  produce  shivering.  Muscle 
sounds  are  especially  common  over  the  pectoralis  major  in  the  anterior 
axillary  region  and  over  the  trapezius  muscle,  (e)  Occasionally  the 
physician  may,  when  the  stethoscope  has  been  placed  in  the  auditory 
meatus,  become  subjectively  conscious  of  his  own  circulatory  sounds. 

In  ausculting  the  chest,  sounds  are  frequently  heard  which  to  the 
beginner,  sound  like  rales.  If  the  patient  swallows  while  one  is  listening 
over  the  chest  the  sound  produced  resembles  very  clearly  that  produced 
by  a  rale.  This  is  especially  apt  to  occur  when  the  patient  coughs  and 
then  takes  a  moderately  deep  breath.  As  this  procedure  is  employed 
especially  to  elicit  latent  rales,  the  patient  should  be  cautioned  not  to 
swallow. 

Occasionally  when  ausculting  the  axillary  regions  fine  rales  are  heard 
during  the  first  moderately  deep  inspiration.  They  are  of  no  significance 
unless  they  persist  during  succeeding  inspiratory  acts. 

At  this  place  mention  might  be  made  of  the  transmission  of  sounds 
from  the  diseased  to  the  healthy  side.  Very  often  the  sound  produced 
by  large  bubbling  or  resonating  rales  as  well  as  exaggerated  voice  sounds 
and  loud  cavernous  or  bronchial  breathing  on  one  side  may  be  heard  on 
the  opposite  side.  When  this  occurs  it  is  always  over  the  upper  and 
posterior  portion  of  the  chest  near  the  large  bronchi.  Mistakes  may  be 
avoided  by  noting  the  character  of  the  percussion  note  and  the  breathing, 
and  especially  by  tracing  the  sounds  from  their  point  of  maximum  inten- 
sity across  to  the  opposite  side.  If  the  sounds  are  not  due  to  bilateral 
lesions  they  will  gradually  diminish  in  intensity. 


THE  INFLUENCE  OF  POSTURE  ON  THE  PHYSICAL  SIGNS 

The  posture  of  the  patient  has  certain  definite  modifying  influences 
upon  the  results  of  the  physical  examination.  A  sitting  position  is 
always  preferable.  If  the  patient  lies  upon  the  side,  percussion  of  the 
lower  lung  yields  a  slightly  impaired  note  with  a  tympanitic  quality. 
The  former  results  from  the  lessened  amount  of  air  which  the  lung  con- 
tains, the  latter  from  diminution  of  pulmonary  tension  and  from  the 
resonating  property  of  the  mattress.  The  resonating  property  of 
extraneous  objects  must  be  borne  in  mind.  For  example,  pulmonary 
resonance  is  greater  if  the  patient  is  percussed  immediately  in  front  of  a 
door  (sounding  board)  then  if  he  stand  in  the  middle  of  the  room.  Slight 
dulness  over  one  pulmonary  apex  which  may  be  readily  demonstrable 
when  the  patient  sits  up,  may  disappear  if  percussion  is  performed  in 
recumbency  while  the  thorax  rests  upon  pillows  or  a  soft  mattress 
(resonators). 

In  the  lateral  decubitus  the  breath  sounds  in  the  lowermost  lung  tend 
to  become  muffled  and  feeble,  owing  to  the  decrease  of  tidal  air.  In  the 
uppermost  lung,  on  the  contrary  their  intensity  may  be  increased. 


AUSCULTATION  107 

THE  STETHOSCOPE 

The  main  functions  of  the  binaural  stethoscope  are  (1)  to  prevent 
lateral  radiation  of  vibrations  with  which  the  air  it  contains,  is  charged, 
thus  conducting  a  larger  proportion  to  the  ear,  and  (2)  to  exclude  extra- 
neous sounds.  A  large  bell  furnishes  more  sound  than  a  small  one,  be- 
cause it  covers  a  larger  area  of  vibration-emitting  surface.  The  bell 
may  also  act  as  a  resonator  and  reinforce  certain  vibrations.  Thus  a 
bell  2  inches  in  diameter  enables  us  to  judge  accurately  regarding  inten- 
sity and  rhythm,  but  is  inferior  to  a  bell  of  ordinary  size  or  to  the  unaided 
ear  in  the  judging  of  equality  and  pitch  (Flint).  Furthermore  it  is 
evident  that  depending  upon  its  shape  and  the  elasticity  of  the  material 
of  which  it  is  made,  the  resonating  quality  of  the  bell  must  vary  consider- 
ably. A  small  bell  is  also  advantageous  since  it  enables  us  to  localize 
sound  more  sharply,  this  being  especially  important  in  ausculting  the 
heart  and  the  supraclavicular  apices,  as  well  as  in  children  and  emaciated 
individuals  in  whom  the  projecting  ribs  interfere  with  close  application 
of  the  bell. 

The  importance  of  the  thoracic  wall  in  acting  as  a  resonator  of  the 
laryngeal  vibrations  has  already  been  alluded  to  under  vocal  fremitus 
(p.  47).  The  sounds  that  we  hear  are  due  to  both  visceral  and  mural 
vibrations.  The  latter  sometimes  preponderate  in  intensity  and  having 
a  lower  pitch  have  a  greater  volume ;  whereas  the  higher  range  due  to  the 
fundamental  note  is  often  medically  of  greater  importance.  Mural 
vibrations  can  to  a  certain  extent  be  eliminated,  and  the  visceral  vibra- 
tions studied  in  isolation  by  exerting  marked  pressure,  with  the  bell  of  a 
a  binaural  stethoscope  equipped  with  rubber  tubing. 

In  case  of  the  mon-aural  stethoscope  made  with  a  hollow  or  solid  stem 
of  metal,  vulcanite  or  wood,  transmission  occurs  both  through  the  stem 
and  through  its  contained  air.  The  thinner  the  walls  of  the  stem  and  the 
bell,  the  more  easily  will  sympathetic  vibrations  be  set  up  and  trans- 
mitted to  the  ear.  A  large  part  of  the  sound  is  thus  transmitted  by  the 
solid  stem.  This  applies  to  a  slight  extent  also  to  the  modern  binaural 
stethoscope,  in  which  some  sound  is  conducted  by  the  rubber  tubing, 
which  tends  to  reinforce  the  aerial  vibrations.  Nor  "is  it  immaterial 
what  thickness  of  tubing  we  employ.  It  must  be  neither  too  flexible 
nor  too  rigid.  High-pitched  sounds  are  conducted  along  tubes,  especially 
soft  tubes  much  less  readily  than  low-pitched  sounds,  because  of  their 
smaller  mass." 

In  using  the  binaural  stethoscope  with  rubber  tubing,  the  results  of 
pressure  on  the  thoracic  wall  are  quite  different.  In  case,  for  instance, 
that  the  bell  is  thick- walled,  and  possessed  of  a  high  fundamental  note 
it  will  be  much  less  affected  by  the  damped  mural  vibrations  than  is  the 
case  with  the  monaural  stethoscope. 

"A  solid  body  laid  upon  the  chest  wall  takes  up  and  transmits  accord- 
ing to  its  own  elastic  properties  the  vibrations  emanating  from  the  latter. 
When  the  pressure  of  the  solid  body  upon  the  surface  is  sufficiently  in- 
creased, the  sensible  vibrations  of  the  latter  are  damped,  but  their  energy 
is,  of  course,  transferred  to  the  body  which  extinguished  them.  When,  for 
example,  the  mon-aural,  solid  stethoscope  is  applied  to  the  chest,  the  sounds 
heard  through  it  are  not  deadened  by  increasing  the  pressure  of  contact; 
on  the  contrary,  the}'  tend  to  become  more  intense,  and  are  brought 


108  THE    EXAMINATION    OF    THE    LUNGS 

nearer  the  ear."1  The  diaphragmatic  type  of  instrument  yields  louder 
sounds  than  a  simple  bell,  because  it  covers  a  large  area  of  sound 
emitting  surface  and  because  the  diaphragm  prevents  the  encroachment 
of  the  soft  tissues  upon  the  lumen  of  the  receiver  (Montgomery).  Per- 
haps also  the  sound  waves  are  amplified  by  the  vibrations  of  the  disc. 
At  all  events,  this  type  of  instrument  should  be  used  as  a  magnifying  lens 
to  study  detail  and,  especially  by  the  beginner,  not  as  the  sole  method 
of  auscultation.  The  sounds  heard  are  not  merely  intensified,  often  they 
are  distorted  because  the  instrument  disproportionately  magnifies  certain 
sounds. 

"Binaural  stethoscopes  and  to  a  minor  degree  phonendoscopes  are 
less  well  adapted  for  the  auscultation  of  faint,  high-pitched  murmurs, 
wheezy  sounds  and  the  metallic  phenomena."1 

Pulmonary  sounds  are  often  heard  better  with  the  unaided  ear, 
applied  directly  to  the  chest  wall,  because  in  such  cases  we  get  bone 
conduction  as  well  as  ear  conduction.  The  early  stages  of  pulmonary 
consolidation,  the  tubular  quality  of  bronchial  breathing,  and  at  times  the 
diastolic  aortic  murmur  are  also  better  appreciated  without  a  stethoscope. 

On  the  other  hand,  the  vesicular  element  of  the  respiratory  murmur, 
heart  sounds  and  generally  speaking  murmurs,  also  certain  rales  are  more 
easily  analyzed  with  a  stethoscope.  This  is  perhaps  due  to  the  fact  that 
certain  wave  lengths  bear  a  definite  reinforcing  relation  to  the  size  of  the 
receiver  and  the  length  of  the  stethoscope  tubing.2 

With  a  small  bell  we  can  localize  more  sharply  but  we  get  less  volume. 
Therefore,  wider  bells  give  better  results  for  feeble  sounds — weak  mur- 
murs, fetal  heart  sounds,  etc.  For  the  latter  deep  pressure  on  the  abdo- 
men is  also  requisite. 

If  a  stethoscope  with  a  spring  is  used,  the  curvature  of  the  metal  parts 
and  ear  pieces  should  correspond  to  that  of  the  external  auditory  meatus, 
since  the  opening  in  the  ear  piece  should  point  directly  toward  the  drum 
and  not  toward  the  cartilaginous  meatus.  Owing  to  differences  in  the  angle 
of  individual  ears,  stethoscopes  with  metal  ear  pieces  must  have  adjust- 
able angulations.  It  is  partly  for  this  reason  that  the  author  prefers 
simple  rubber  tubing  without  any  spring  attachment  whatever. 

The  Choice  of  a  Stethoscope. — This  is  largely  a  question  of  personal 
preference.  A  small  minority  still  prefer  the  mon-aural  type,  perhaps  as 
a  matter  of  habit.  Certainly  two  ears  are  better  than  one,  especially 
when  one  is  hampered  by  extraneous  noises.  In  a  choice  between  many 
binaural  types  certain  factors  must  be  considered: 

1.  The  ear  pieces  must  fit  the  external  auditory  meatus  exactly,  not 
only  in  order  to  exclude  outside  noises,  but  also  so  that  the  instrument 
can  be  used  indefinitely  without  discomfort  or  pain.  A  little  time  con- 
sumed in  filing  the  ear  pieces  to  the  proper  shape  and  dimensions  is  well 
spent. 

2.  Instruments  of  the  phonendoscope  type — those  with  diaphragms 
■ — should  never  be  used  by  beginners.  They  not  only  magnify,  but  also 
distort,  sounds.  Their  habitual  use  even  by  more  experienced  clinicians 
establishes  a  false  standard  of  normality,  and  often  renders  the  examiner 
more  or  less  helpless  in  case  they  are  temporarily  unavailable. 

1  Sewall,  Henry:  "The  Role  of  the  Stethoscope  in  Physical  Diagnosis."  Amer. 
Jour.  Med.  Sci.,  February,  1913,  p.  234. 

2  Conner:  N    Y.  Med.  Jour.,  July  13,  1907. 


AUSCULTATION  109 

3.  The  tubing  should  not  be  smaller  than  the  caliber  of  the  metal 
parts,  and  should  be  sufficiently  heavy  to  prevent  kinking. 

4.  An  extra  bell  (receiver)  smaller  than  the  usual  size  is  desirable, 
especially  in  the  practice  of  pediatrics. 

5.  The  instrument  should  be  light  and  compact  so  that  it  can  be 
readily  carried  in  the  pocket. 

The  author  personally  prefers  the  Sansom  instrument  with  two  bells, 
and  furnished  with  an  extra  diaphragmatic  receiver  for  occasional  use. 

THE  BREATH  SOUNDS 

The  act  of  breathing  causes  certain  sounds  which  are  known  as  the 
breath  sounds  or  the  respiratory  murmur.  The  breath  sounds  may  be 
heard  when  the  ear  is  applied  to  an  area  of  the  thorax  overlying  lung- 
tissue.  They  are  composed  of:  (1)  the  laryngeal  or  ''bronchial,"  and 
(2)  the  vesicular  elements. 

The  Laryngeal  Element. — During  both  inspiration  and  expiration 
certain  sounds  are  produced  in  the  nose,  mouth,  glottis,  larynx  and 
trachea.  They  are  clue  to  sonorous  vibrations  caused  by  a  column  of 
air  moving  through  the  structures  in  question  (Fig.  96). 

If  we  listen  over  the  trachea  during  the  act  of  respiration  we  generally 
hear  high-pitched  sounds,  having  a  tubular  quality,  with  expiration 
lasting  as  long  or  longer  than  inspiration;  the  former  having  a  higher 
pitch  than  the  latter  and  being  separated  from  it  by  a  distinct  interval. 
When  we  listen  over  the  lung  these  sounds  have  undergone  a  great  modi- 
fication. The  sounds  are  softer,  lower  in  pitch,  expiration  is  very  short, 
and  faint,  indeed  often  it  is  inaudible,  while  the  pause  separating  inspira- 
tion has  practically  disappeared. 

Stenosis  of  any  portion  of  the  upper  respiratory  tract,  such  as  by  nasal 
or  faucial  adenoids,  markedly  increases  the  intensity  of  the  laryngeal 
element  of  the  respiratory  murmur.  Such  obstruction  may  cause 
broncho-vesicular  breathing  over  the  pulmonary  apices,  thus  simulating 
infiltration  of  the  lung.  It  is  to  be  distinguished  from  the  latter  by  its 
bilateral  character,  disappearance  when  the  obstruction  is  removed  and 
by  the  absence  of  percussion  dulness  (Fig.  95). 

The  primary  sound  producing  vibration  in  the  respiratory  system 
arises  in  the  vibrations  of  tissues,  not  of  the  air.  The  moving  air  sets 
the  tissues  in  motion ;  this  produces  a  sound,  which  is  in  turn  conveyed  or 
conducted  by  the  air,  as  well  as  by  the  tissues  which  surround  them — 
the  bronchi  and  pulmonary  tissue. 

The  relationship  is  that  of  the  bow,  to  the  violin  string,  the  former  being 
represented  by  the  air  current,  the  latter  by  the  tissues.  Furthermore, 
the  rapidity  of  the  current  affects  the  intensity  of  the  sounds  (amplitude 
of  the  vibrations).  When  the  air  current  is  rapid,  more  intense  breath 
sounds  are  produced.  Just  as  the  voice  sounds  produced  in  the  larynx 
are  carried  downward  into  and  through  the  pulmonary  tissues,  so  are  the 
breath  sounds,  which  arise  at  the  same  source. 

"The  chief  effect  of  the  bronchial  walls  is  to  prevent  diffusion,  thus 
allowing  the  good  conducting  properties  of  the  air  to  operate  at 
advantage." 

The  voice  and  breath  sounds  lose  much  of  their  intensity  as  we  hear 
them  over  the  chest  wall,  (1)  as  a  result  of  diffusion,  although  this  loss 


110  THE    EXAMINATION    OF    THE    LUNGS 

is  more  or  less  offset  by  the  deep  penetration  of  the  bronchi  into  the 
pulmonary  tissue;  (2)  owing  to  reflection  which  occurs  when  the  air- 
borne vibrations  pass  through  the  walls  of  the  bronchi;  (3)  because  in 


Fig.  96. — This  anteroposterior  section  through  the  head  and  thorax  depicts  the  struc- 
tures concerned  in  the  production  and  modification  of  the  "laryngeal"  element  of  the  breath 
sounds. 

Auscultation  over  the  area  "A"  during  nasal  breathing,  the  mouth  being  closed,"»yields 
pure  cavernous  breathing  (low-pitched  sounds  with  a  hollow  or  reverberating  quality,  and 
expiration  longer  than  inspiration).  The  outgoing  air  strikes  the  nares  more  directly  than 
when  the  mouth  is  open;  the  vocal  cords  are  more  closely  approximated  during  expiration 
and  vibrate  considerably.  The  nares  and  the  mouth  furnish  the  cavity  for  the  reverbera- 
tion of  sound,  and  the  occipital  bone  is  a  good  conductor. 

Auscultation  over  the  area  "  B."  If  the  mouth  is  open,  the  air  passes  directly  out  of  it, 
the  nasal  resonator  has  been  eliminated  and  the  cavernous  quality  as  well  as  the  intensity  of 
the  breath  sounds  almost  entirely  disappear.  The  results  of  tracheal  auscultation  are  also 
greatly  modified  by  oral  and  nasal  breathing.      (Barach.) 

passing  from  the  bronchial  walls  into  the  pulmonary  septa  more  wave 
energy  is  lost  by  reflection;  (4)  as  similar  loss  occurs  in  passing  through 
the  air  chambers  of  a  normally  distended  lung;  (5)  since  they  meet  with 
reflection  again  in  passing  from  the  lung  to  the  chest  wall,  because  here 


AUSCULTATION  111 

again  a  distinct  "break"  occurs  in  passing  from  a  very  light  to  a  fairly 
heavy  medium,  as  well  as  (6)  diffusion  in  passing  through  the  chest  wall. 

The  breath  sounds  as  heard  over  the  chest  become  altered  from  the 
character  they  possess  at  their  source  of  origin  in  regard  to  intensity, 
quality  and  pitch.  The  change  in  intensity  results  mainly  from  diffusion 
and  reflection  although  absorption,  resonance,  and  perhaps  interference 
also  plays  a  part.  "  Changes  in  pitch  and  quality,  although  explicable 
to  some  extent  in  the  elimination  of  the  weaker  vibrations  as  the  whole 
sound  becomes  more  feeble,  appear  to  be  due  chiefly  to  the  factors  of 
resonance  and  interference  affecting  certain  vibrations,  while  exerting 
little  or  no  influence  on  other  vibrations  which  go  to  form  the  complex 
group  of  vibrations  which  we  ordinarily  term  a  single  sound" 
(Montgomery)  ("see  p.  59). 

The  Vesicular  Element. — In  addition  to  the  laryngeal  sound  just 
described,  a  vesicular  element  is  added  which,  when  auscultation  is 
practised  over  the  chest,  furnishes  most  of  the  inspiratory  pulmonary 
breath  sound.  It  is  due  to  the  separation  and  distention  of  the  alveoli 
by  the  inrushing  current  of  air.  The  expiratory  portion  appears  to  arise 
in  the  upper  respiratory  tract.  The  fact  that  the  sound  heard  over  the 
chest  wall  is  more  muffled,  weaker  and  lower  in  pitch  than  that  audible 
experimentally  over  the  actual  periphery  of  the  lung  is  due  to  loss  of 
vibratory  intensity  in  passing  from  the  lung  to  the  chest  wall  and  from 
the  chest  wall  to  the  stethoscope  (vibratory  reflection). 

The  Basis  for  the  Assumption  of  Alveolar  Sound  Production. — The 
cubic  capacity  of  an  alveolus  is  0.00494  mm.   (Zuntz). 

In  long-necked  animals,  such  as  the  ruminants,  the  respiratory  murmur  is  much 
less  loud  than  in  the  short-necked  ones,  such  as  the  carnivora. 

The  estimated  total  of  the  alveoli  is  400  million.  As  the  average  lung  volume  is 
4000  cm.,  1  cm.  would  include  100,000  alveoli.  If  we  assume  that  in  ausculting  we 
hear  sound  from  a  depth  of  3  cm.,  we  would  perceive  sound  yielded  by  half  a  sphere  14 
cm.  in  circumference.  In  other  words,  we  would  hear  the  combined  sound  of  1,400,000 
alveoli.  Since  a  normal  deep  inspiration  takes  2  seconds,  we  should  hear  the  sound  of 
700,000  alveoli  per  second.  Now  we  cannot  recognize  as  separate  sounds,  vibrations 
occurring  with  a  rapidity  of  700  per  second,  as  would  be  the  case  if  1000  alveoli  gave 
forth  sound  simultaneously.  But  alveolar  distention  is  gradual  and  when  a  sufficient 
number  of  sequent  groups  produce  sound,  it  is  extremely  plausible  to  assume  that  an 
audible  sound  is  thus  engendered. 

Only  on  such  a  hypothesis  can  we  assume  that  sound  is  produced  in  the  alveoli. 

The  dimensions  of  an  alveolus  are  so  small  that  there  is  no  possibility  of  sound 
production  after  the  manner  in  which  it  occurs  in  the  trachea  or  bronchi.  "There 
can  be  no  question  of  inspiratory  vibration,  reflexion,  interference,  or  the  formation 
of  horizontal  waves  where  there  is  no  reflective  wall  because  the  relationship  between 
the  size  of  the  waves  and  the  chambers  is  too  disproportionate"  (Geigel,  p.  172). 

"The  total  alveolar  surface  of  the  lung  amounts  to  no  less  than  90  square  meters, 
or  100  times  the  body  surface."1  The  interlobar  bronchioles  end  in  narrow  alveolar 
ducts  and  these  "expand  in  turn  into  comparatively  wide  infundibuli  lined  by  air 
cells.  This  sudden  widening  out  of  the  air  passage  is  believed  to  aid  in  the  produc- 
tion of  the  inspiratory  sound  heard  in  ausculting  the  lungs,  eddies  being  set  up  in 
the  passage  of  the  air  from  the  narrower  to  the  wider  cavity"  (Hutchison). 

Sahli  found  in  a  case  of  pulmonary  hernia  due  to  a  sternal  fissure  that  character- 
istic vesicular  breathing  could  be  heard  over  the  hernia  during  the  performance  of  the 
Valsalva  experiment,  in  which  of  course  all  laryngeal  and  glottic  sounds  were  elimi- 
nated, and  proving  that  at  least  a  part  of  the  vesicular  sound  originated  in  the  ves- 
icles themselves.  The  vesicular  sound  is  also  noted  in  cases  of  cardio-pulmonary  mur- 
murs, a  factor  which  further  corroborates  the  foregoing  statement  (Sahli,  Corre- 
spondenzblatt  f.  Schweizer  Aertze,  1892). 

1  R.  Hutchison:  "Applied  Physiology,"  1908. 


112  THE    EXAMINATION    OF    THE    LUNGS 

The  greater  part  of  the  expiratory  sound  is  produced  by  the  passage 
of  air  over  the  vocal  cords  and  through  the  glottis.  It  contains,  as  well, 
certain  sounds  arising  in  the  oral  and  nasal  cavities  and  some  contributed 
by  the  trachea  and  the  bronchi. 

The  greater  part  of  the  inspiratory  portion  arises  in  the  vesicles.  In 
as  much,  therefore,  as  both,  but  especially  the  expiratory  portion,  have  a 
composite  genesis  it  is  not  surprising  to  find  that  the  breath  sounds  heard 
over  the  chest  may  vary  in  different  individuals,  and  even  in  the  same 
person  under  varying  conditions,  in  regard  to  intensity,  quality,  dura- 
tion and  pitch. 


CHAPTER  IX 
NORMAL  AND  ABNORMAL  BREATH  SOUNDS 

THE   NORMAL   VESICULAR   SOUND 

The  sound  normally  heard  over  pulmonary  tissue  during  the  act  of 
breathing — the  vesicular  murmur — is  regular  in  rhythm,  low  in  pitch,  and 
soft,  breezy  or  rustling  in  character.  It  is  heard  throughout  respiration, 
but  progressively  diminishes  in  intensity  during  expiration,  the  end  of 
which  is  inaudible.  There  is  only  a  very  brief  pause  between  in-  and 
expiration.  It  is  to  be  noted  that  although  the  duration  of  these  two 
physiologic  phases  of  respiration  is  as  5  to  6,  the  audible  duration  is  as 
5  to  1,  respectively.  In  other  words  the  expiratory  sound  is  much  shorter 
than  that  of  inspiration,  and  sometimes  it  is  barely  audible.  Being  a  purely 
passive  act,  which  results  from  the  elastic  recoil  of  the  distended  lung 
tissue,  it  is  less  harsh,  and  lower  in  pitch,  as  well  as  shorter  than  inspira- 
tion. The  elastic  recoil  is  greatest  at  the  end  of  inspiration,  hence 
the  beginning  of  expiration  is  more  intense  than  its  end.  Furthermore, 
the  glottis  is  more  widely  opened  during  inspiration  and  the  air  leaves 
the  chest  less  rapidly  than  it  enters.  The  vesicular  sound  may  be 
imitated  by  breathing  deeply  with  the  lips  set  in  the  position  which  pro- 
duces a  soft  "F."  In  ausculting  the  lungs,  the  beginner  especially, 
should  note  the  character  of  the  expiration,  for  it  is  in  this  phase  particularly 
that  pathologic  abnormalities  are  most  apt  to  occur. 

ABNORMAL  BREATH  SOUNDS 

The  vesicular  murmur  may  become  abnormal  owing:  (1)  to  a  change 
in  its  character  (intensity,  quality,  duration,  pitch  or  rhythm) ;  or  (2)  to 
the  introduction  of  new  or  adventitious  sounds,  i.e.,  (a)  rales;  (b)  fric- 
tions; (c)  succussion  splash;  (d)  metallic  tinkle. 

THE  CLASSIFICATION  OF  ABNORMAL  BREATH  SOUNDS 

Abnormal  breath  sounds  are  more  or  less  arbitrarily  classified  as  (1) 
exaggerated,  (2)  broncho-vesicular,  (3)  bronchial,  (4)  cavernous,  and  (5) 
amphoric. 

Changes  in  the  Intensity  and  Quality  of  the  Breath  Sounds. — Exagger- 
ated Breathing. — (a)  A  mere  increase  in  the  intensity  of  the  respiratory 
murmur  is  known  as  exaggerated  breath  sounds,  and  is  due  to  increased 
vesicular  activity — more  air  entering  in  a  given  unit  of  time  than  is  nor- 
mally the  case.  Such  a  condition  is  normal  in  children,  hence  the  name 
puerile  breathing.  It  may  occur  in  any  individual  who  is  breathing  hard, 
as  for  instance  after  physical  exertion.  In  women  the  respiratory  sounds 
are  louder  than  in  men,  especially  in  the  upper,  anterior  thoracic  region, 
and  during  expiration  (costal  breathing).  In  exaggerated  breathing 
both  in-  and  expiration  are  harsh  and  prolonged  because  the  glottic 
8  113 


114 


THE    EXAMINATION    OF    THE    LUNGS 


sounds  are  louder  and  on  account  of  the  increased  pulmonary  tension 
(vicarious   "emphysema ") . 

(b)  Decreased  breath  sounds  (feeble,  senile,  emphysematous,  breath 
sounds)  are  characterized  by  the  fact  that  the  sounds  are  faint  or  short; 
expiration  may  be  inaudible.  This  may  be  due  to :  (1)  diminished  sound 
conduction — bronchial  obstruction  (increased  diffusion  and  reflection) — 
pleural  effusion  or  thickening  (increased  reflection)  cutaneous  adiposity 
or  edema,  etc.;  or  to  (2)  diminished  sound  production — shallow  breath- 
ing arising  from  pain,  muscular  weakness,  thoracic  rigidity,  pulmonary 
emphysema. 


Fig.  97. — Diagram  to  illustrate  the  occurrence  and  non-occurrence  of  bronchial 
breathing  in  pneumonia.  On  the  right  side  the  consolidation  spreading  inward  has 
reached  the  bronchus  and  as  a  result  bronchophony  and  bronchial  breathing  are  heard. 

On  the  left  side  there  is  still  a  break  in  the  continuity  of  consolidation  between  the 
periphery  and  the  large  tubes,  and  although  dulness  is  marked,  bronchial  breathing  and 
bronchophony  are  absent.  The  breath  sounds  are  feeble  or  absent.  This  partial  or  entire 
suppression  of  the  breath  sounds,  especially  of  the  vesicular  element,  associated  with  percussion 
dulness,  and  occasional  rales  on  deep  breathing,  occurs  in  the  early  days  of  a  pneumonia  much 
more  frequently  than  bronchial  breathing. 

In  the  early  stages  of  pneumonia  and  of  pulmonary  tuberculosis  the 
sounds  are  often  indistinct  and  muffled. 

(c)  Breath  sounds  may  be  absent  in  pleural  effusion,  closed  pneumotho- 
races  with  atalectasis,  or  from  occlusion  of  a  bronchus — pressure  or 
exudation.  "Diffusion  of  sound  between  the  lung  surface,  free  from 
adhesions,  and  the  chest  wall,  shares  the  honors  with  reflection  of  sound 
from  the  fluid  back  into  the  air  in  the  lung,  in  reducing  the  intensity  of 
sounds  in  their  passage  from  lung  to  chest  wall  in  ordinary  cases  of  pleural 
effusion  "  (Montgomery) . 


NORMAL  AND  ABNORMAL  BREATH  SOUNDS  115 

Pleural  effusions  sometimes  yield  normal  or  actually  increased 
fremitus,  voice  and  breath  sounds  even  below  the  level  of  the  fluid. 

This  phenomenon  is  ascribed  by  Montgomery  to  the  fact  that  the  lung  is 
solid  either  as  the  result  of  exudation,  infiltration  or  compression  and 
being  such  imparts  its  vibrations  readily  to  the  surrounding  fluid  without 
much  of  a  "break"  due  to  reflection.  This  state  of  affairs  is  only  inade- 
quately offset  by  the  loss  of  sound  through  diffusion  in  the  effusion,  so 
that  the  end  result  is  at  least  "normal"  if  not  actually  an  increased  inten- 
sity of  transmission.  A  similar  effect  although  less  in  degree  may  be 
exerted  upon  fluid  by  a  collapsed  lung.  It  is  furthermore  evident  that 
anything  which  tends  to  bring  the  lung  near  to  the  chest  wall — adhesions, 
large  lungs  and  small  thoraces  (in  infants) — would  further  tend  to  prevent 
the  disappearance  of  fremitus,  resonance  and  breath  sounds,  in  cases  of 
pleural  effusion. 

Broncho -vesicular  Breathing. — This  is  a  combination  of  the  vesicular 
and  the  bronchial  types,  both  the  soft  vesicular  and  the  harsh  bronchial 
elements  being  present,  either  one  of  which  may  predominate.  Some 
authorities  prefer  to  use  the  term  vesiculo-bronchial  if  the  vesicular 
sound  is  preponderant,  and  broncho-vesicular  when  the  bronchial  sound 
is  the  greater.  Others  prefer  to  include  both  these  types  under  one  head- 
ing, and  modify  the  term  by  adding  such  adjectives  as  slight,  marked, 
harsh,  intense,  etc. 

Physiologic  broncho-vesicular  breathing  is  heard  over  definite  locations 
at  which  it  is  normal  and  can  be  explained  on  anatomic  grounds.  It  is 
considerably  influenced  by  opening,  narrowing  or  closing  the  mouth  or 
the  glottis;  and  tends  to  become  more  intense  as  a  main  bronchus  is  ap- 
proached. The  pathologic  type  of  broncho-vesicular  breathing  may  occur 
over  any  portion  of  the  lung  and  is  relatively  uninfluenced  by  alterations 
in  the  oral  resonator  (breathing  through  the  mouth  or  nose).  It  occurs 
when  both  normal  vesicles  and  infiltrated  pulmonary  tissue  exist  together, 
as  in  incomplete  consolidation. 

Bronchial  Breathing. — By  this  term  which  is  synonymous  with  tubular 
breathing,  we  understand  a  loud,  harsh,  high-pitched,  snorting  type  of 
breath  sound,  with  a  distinct  pause  between  inspiration  and  expiration,  the 
latter  being  even  longer,  more  harsh  and  higher-pitched  than  the  former. 
The  soft,  low-pitched,  rustling  or  breezy  vesicular  element  is  entirely 
absent.  The  breath-sounds  normally  heard  over  the  trachea  are  often 
used  as  an  example  of  bronchial  breathing,  but  the  tracheal  sound  is 
generally  more  harsh  and  lower  in  pitch  than  that  which  occurs  patho- 
logically over  consolidated  lung  tissue.  As  in  normal  breathing,  the 
primary  sound  originates  in  the  upper  respiratory  tract.  Bronchial 
breathing  is  characteristic  of  consolidated  lung  because  conditions 
are  less  unfavorable  for  sound  transmission  than  is  the  case  in  normal 
lungs.  The  vibrations  pass  from  the  bronchial  wall  to  the  surrounding 
consolidated  lung  and  thence  to  the  chest  wall  without  undergoing  a 
serious  "break"  in  the  process  of  transmission.  This  is  so  because 
bronchus,  solid  lung  and  chest  wall  are  acoustically  more  or  less  identical 
and  there  is,  therefore,  not  much  chance  for  diffusion  or  reflection  of  the 
vibrations  at  the  different  tissue  junctions. 

Montgomery  has  shown  that  lung  under  normal  tension  transmits 
sound  much  less  well  than  either  relaxed  or  consolidated  pulmonary  tissue. 
"The  occurrence  of  weaker  sounds  over  the  normal  chest  than  over  the 


116 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.  98. 


Figs.  98  and  99. — These  figures  illustrate  the  areas  over  which  breath  sounds  are  nor- 
mally harsh.  The  terrn  vesiculo-bronchial  as  here  used  signifies  vesicular  breathing  with  a 
very  slight  degree  of  the  bronchial  element.  In  other  words,  the  sound  heard  is  just  a  trifle 
more  harsh  and  high  pitched  than  over  the  corresponding  area  on  the  opposite  side.  The 
degree  of  harshness  which  is  subject  to  considerable  individual  variation,  is  mainly  due  to 
the  proximity  of  the  right  upper  lobe  to  the  trachea  anteriorly,  and  posteriorly,  in  addition, 
to  the  tracheal  bifurcation.      (Compare  Figs.  49,  52,  75,  95,  104.) 


NORMAL  AND  ABNORMAL  BREATH  SOUNDS 


117 


chest  where  there  is  consolidation  is  due  not  only  to  favorable  conditions 
on  the  diseased  side,  but  also  to  unfavorable  transmission  facilities  on  the 
normal  side.  These  are  the  main  factors  in  explaining  why  the  side  con- 
taining the  larger  amount  of  air  yields  weaker  sounds,  than  that  containing 
the  greater  amount  of  solid  tissue,  at  the  periphery  of  the  chest." 

The  term  bronchial  breathing  is  sanctioned  by  usage,  but  is  not 
descriptive  as  signifying  the  sound  normally  heard  over  the  bronchi. 

The  type  of  bronchial  breathing  heard  above  and  sometimes  directly 
over  pleural  effusions  has  a  similar  genesis  and  is  due  to  associated  com- 
pression or  consolidation  of  the  lung. 

Bronchial  breathing  occurs  characteristically  over  large  areas  of 
complete  pulmonary  consolidation  such  as  in  pneumonia.  It  frequently 
is  not  demonstrable  until  the  third  or  fourth  day  after  the  onset.     The 


Pure  bronchial 


Broncho- 
vesicular 
(incomplete 
consolida- 
tion) 


Fig.  100. 


-Diagram  illustrating  different  types  of  tbe  breath  sounds  in  various 
pathologic  conditions. 


consolidation  begins  at  the  periphery  and  gradually  spreads  inward 
toward  the  hilus  and  although  dulness  occurs  quite  early,  bronchial 
breathing  and  bronchophony  do  not  appear  until  the  entire  fan-shaped 
area  of  lung  tissue  lying  between  the  pleura  and  the  large  bronchi  has 
become  consolidated  (see  Fig.  97). 

Bronchial  breathing  is  never  heard  over  normal  lung  tissue.  It  may  be 
imitated  by  a  harshly  whispered  "Ha"  or  by  a  guttural  "Ch." 

Cavernous  Breathing. — This  type  of  breathing  may  be  heard  over 
cavities  and  open  pneumothoraces.  It  is  low  in  pitch,  and  has  a  hollow 
reverberating  quality.  Frequently  the  expiration  is  even  lower-pitched 
than  the  inspiration,  the  relations  of  bronchial  breathing  being  thus 
reversed.  As  pointed  out  by  Flint,  it  is  more  apt  to  be  confused  with 
normal  vesicular  breathing,  than  with  the  bronchial  type,  and  is  to  be 
differentiated  from  the  former  "only  by  the  absence  of  the  vesicular 


118 


THE    EXAMINATION    OF    THE    LUNGS 


quality  in  the  inspiratory  sound''  (Flint).  The  expiration  is  always  pro- 
longed and  puffing  (Loomis).  Phonetic  equivalent  =  whispered  "Who." 
Some  authors  deny  the  existence  of  cavernous  breathing  altogether, 
classing  it  as  a  variety  of  bronchial  breathing — low-pitched  bronchial. 
Cavernous  breathing  may  be  imitated  by  breathing  into  the  hollowed 


|lji  U  ifei  ^!!  j  111-  Sj.i^i  .2+ 

?->'z  =  a  *J>-  g|  -r£=-     a  a  a  J  °"i     i>"=  ="?  -  =  o  3  -  <a  -  y-  §  P 

iriiis i mini y~i i  i+i y  1  l^lll lilt 


d  —    Fh    O    rn 


hands.     It  is  heard  normally  over  the  occiput,  especially  if  the  mouth  be 
closed  (see  Fig.  96). 

Like  bronchial  breathing,  cavernous  breathing  has  its  origin  in  the 
upper  respiratory  tract.  In  the  former,  however,  we  are  dealing  not 
merely  with  ordinary  bronchi  but  also  with  excavations  which  possess 
resonating  properties. 


NORMAL  AND  ABNORMAL  BREATH  SOUNDS  119 

Only  rarely  is  the  genesis  of  this  sound  due  to  the  fact  that  the 
respiratory  air  current  actually  enters  a  cavity  and  sets  up  vibrations 
within  it.  What  generally  occurs  is  that  vibrations  in  the  neighborhood 
of,  and  external  to  the  cavity,  set  up  sympathetic  vibrations  within  the 
cavity,  which  then  acts  as  resonator,  reinforcing  and  modifying  the  original 
sound;  imparting  to  it  the  hollow  reverberating  quality  which  we  recog- 
nize as  "cavernous"  or  the  higher-pitched  metallic  sound  which  we  desig- 
nate as  amphoric  breathing. 

Amphoric  Breathing. — This  is  a  high-pitched  form  of  cavernous  breath- 
ing, with  high  ringing  overtones  which  impart  a  metallic  quality.  It  may 
be  heard :  over  tense,  smooth,  stiff-walled  cavities,  in  size  not  less  than  a 
walnut,  especially  if  superficially  placed;  and  over  pneumothoraces. 
It  is  analogous  to  the  metallic  ring  of  percussion  (see  p.  69). 

If  we  blow  into  a  cylinder  such  as  a  test-tube,  in  such  a  way  as  to  cause  sound  waves 
by  reflection,  we  get  a  strong  fundamental  note,  with  weak  harmonious  overtones,  but 
if,  as  with  the  bottle  we  add  a  neck  relatively  small  in  proportion  to  the  size  of  the 
cylinder,  and  sufficiently  long,  we  get  a  peculiar  high  metallic  quality.  This  is  the 
result  of  unrhythmic  vibrations,  due  either  to  the  angle  of  reflection  or  to  the  force  of 
the  blow,  by  virtue  of  which  the  air  in  the  lee  of  the  neck  (see  Fig.  102)  does  not  begin 
to  vibrate  until  after  that  beyond  has  been  set  in  vibration.  In  the  former  instance 
we  produce  cavernous,  in  the  latter  amphoric,  sounds. 

Amphoric  sounds  may  be  heard  over  a  closed  cavity,  or  a  closed 
pneumothorax;  in  these  cases  the  metallic  quality  is  due  to  a  quick,  local 
percussion  of  their  walls  by  means  of  the  neighboring  air  columns. 

Although  amphoric  breathing  is  more  intense,  and  generally  of  higher 
pitch  than  cavernous  breathing,  the  essential  difference  lies  in  the  metallic 
quality  of  the  former.     If  we  blow  softly  across  the  neck  of  a  bottle  the 


Fig.  102. — Diagram  illustrating  the  production  of  metallic  breath  sounds — amphoric 
breathing — in  large  stiff-walled  cavities. 

sound  will  be  cavernous,  if  intensely  it  becomes  amphoric.  The  pitch 
depends  on  the  length  of  the  air  columns  and  on  the  size  of  the  opening. 
The  metallic  quality  depends  on  the  generation  of  very  unrhythmic 
vibrations — on  the  suddenness  of  the  entrance  or  impact  of  the  vibrations. 
It  is  for  this  reason  that  the  amphoric  quality  is  often  only  apparent  dur- 
ing forcible  breathing,  just  as  a  metallic  percussion  note,  and  cracked-pot 
sound  can  generally  only  be  elicited  by  quick,  forcible  percussion. 

Metamorphic  Breathing. — This  term  is  sometimes  applied  to  different 
varieties  of  mixed  breath  sounds.  Thus,  breath  sounds  with  a  feeble 
indistinct  beginning  may  end  as  the  pure  bronchial  type,  or  the  pitch  of 
the  bronchial  element  may  change,  or  inspiration  may  begin  as  a  broncho- 
vesicular  and  end  as  an  amphoric  sound.  The  change  is  generally  attrib- 
uted to  opening  of  an  occluded  or  occlusion  of  an  open  bronchus. 

Asthmatic  Breathing. — This  form  of  the  respiratory  murmur  is  heard 
during  paroxysms  of  asthma,  frequently  in  emphysematous  subjects. 
Both  inspiration  and  expiration  are  increased  in  intensity,  especially  the 
latter,   which  is  high-pitched,   prolonged  and  wheezing  in  character,  and 


120 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.  103. — Cardiac  Hydro-thorax.  A  case  of  rheumatic  mitral  and  tricuspid  disease, 
with  marked  cardiac  dilatation,  auricular  fibrillation,  etc.,  under  observation  for  many  rears. 
Died  in  a  state  of  anasarca.     Body  frozen  in  the  recumbent  posture. 

The  diaphragm  is  depressed.  The  effusion  reaches  to  the  uppermost  limits  of  the 
pleural  cavity.     The  lung  is  compressed,  and  the  dilated  heart,  displaced  downward. 

The  pericardium  contains  a  small  effusion.     The  following  physical  signs  were  noted: 

Over  the  back  and  the  sides  of  the  chest:  A  flat  percussion  note,  with  absent  vocal  frem- 
itus and  resonance  and  breath  sounds.  Over  the  front  of  the  chest:  A  short,  high-pitched, 
slightly  tympanitic  note  (Skodaic) ;  exaggerated  breath  sounds,  increased  vocal  fremitus 
and  resonance  (compression) ;  subcrepitant  rales  (congestion  and  serous  exudation) ;  in  some 
areas  distant  broncho-vesicular.  In  others  suppressed,  breath  sounds,  (compression  of 
vesicles  or  of  bronchi).     In  the  upper  anterior  axillary  line  egophony  was  elicited. 


NORMAL  AND  ABNORMAL  BREATH  SOUNDS  121 

generally  associated  with  musical  rales.     It  is  frequently  audible  at  a 
distance  from  the  patient. 

CHANGES  IN  RESPIRATORY  RHYTHM 

Cog-wheel  Respiration. — In  this  type  of  breathing,  inspiration  in- 
stead of  producing  a  soft,  continuous  sound,  as  is  normally  the  case,  is 
interrupted,  so  that  it  occurs  as  a  series  of  jerks  or  puffs  and  pauses. 
This  occurs  chiefly  in  the  upper  lobes  or  at  the  anterior  margins  of  the 
lungs.  It  is  clue  to  irregular  inflation  and  expansion  of  the  pulmonary 
lobules.  It  may  result  from  pleural  adhesions  and  is  a  frequent  phe- 
nomenon in  tuberculous  cases,  but  may  also  occur  as  a  result  of  asthma, 
pain  or  fatigue  of  the  respiratory  muscles.  (For  visible  changes  in 
respiratory  rhythm  see  p.  41.)  It  is  sometimes  met  with  in  healthy 
people  with  apparently  normal  lungs. 


CHAPTER  X 
ADVENTITIOUS  BREATH   SOUNDS 

raxes  and  frictions 

Rales  are  more  or  less  musical  sounds  which  originate  in  the  vibration 
of  exudate  in  the  respiratory  passages.  The  exudate  practically  acts 
like  a  reed  in  a  wind  instrument.  Genetically  all  rales  are  moist,  but 
sometimes  they  are  classified  as  " moist"  and  "dry."  These  are 
undesirable  terms  however,  and  should  not  be  used. 

If  a  rale  is  described  simply  as  a  "dry  rale"  or  a  "mucous  rale"  it  connotes  nothing 
definite  and  further  is  not  along  the  lines  of  scientific  accuracy.  Further,  the  term 
"dry"  as  applied  to  rales  seems  paradoxical,  for  it  is  almost  impossible  to  conceive  of  a 
"rale"  that  does  not,  to  some  extent  at  least,  depend  on  moisture  or  increased  tumes- 
cence for  its  causation. 

Rales  vary  in  quality,  size,  pitch,  time,  intensity,  duration,  distribu- 
tion, according  to  the  size  of  the  air  chambers  (bronchi-bronchioles)  and 
the  character  of  the  exudate. 

Rales  are  arbitrarily  classed  in  five  groups,  a  classification  based  on 
their  primary  auditory  characteristics. 

1.  Sonorous  rales,  loud,  snoring  and  low-pitched. 

2.  Sibilant  rales,  whistling,  piping,  squeaking,  hissing,  humming. 
High-pitched. 

These  two  varieties  constitute  what  is  known  as  the  musical  rales. 
Their  sound  is  longer  and  more  continuous  than  that  of  the  other  varieties. 
They  are  generally  caused  by  a  thin,  tenacious  exudate,  and  are  most 
characteristically  heard  in  cases  of  asthma.  They  are  considerably 
influenced  by  coughing. 

3.  Crepitant  rales  are  very  fine,  chiefly  inspiratory,  constant,  clear- 
cut,  high-pitched,  uninfluenced  by  coughing,  probably  alveolar  in  origin. 
They  are  also  known  as  consonating  rales.  They  are  heard  in  associa- 
tion with  bronchial  breathing,  and  seem  to  originate  close  to  the  ear. 
They  may  be  imitated  by  rubbing  a  lock  of  hair;  or  by  separating  the 
fingers,  which  have  been  moistened  by  saliva.  They  often  have  a 
metallic  quality,  especially  when  associated  with  cavitation,  or  consolida- 
tion. They  may  be  heard  in  the  early  and  the  late  stages  of  pneumonia 
(crepitus  indux  and  redux).  Also  in  broncho-pneumonia,  infarction, 
pulmonary  tuberculosis.  They  are  the  only  rales  produced  in  the  alveoli 
and  indicate  parenchymatous  involvement  of  the  lung. 

4.  Subcrepitant  (Crackling)  Rales. — These  are  coarser  and  lower- 
pitched  than  crepitant  rales.  They  may  be  simulated  by  rolling  a  dry 
cigar  between  fingers,  or  sprinkling  salt  on  a  hot  stove.  They  originate 
in  the  bronchi  and  bronchioles,  and  are  heard  in  cases  of  bronchitis, 
pulmonary  congestion  and  edema.  Crepitant  and  crackling  rales  may 
be  closely  simulated  by  friction  sounds. 

122 


ADVENTITIOUS  BKEATH  SOUNDS 


123 


5.  Bubbling  and  Gurgling  Rales. — These  are  also  known  as  mucous, 
or  liquid  rales.  They  are  coarser  and  lower-pitched  than  crackling 
rales.  They  are  generally  heard  over  the  large  bronchi,  or  cavities,  and 
in  cases  of  pulmonary  edema.  The  so-called  "death  rattle"  is  due  to 
liquid  exudation  in  the  trachea,  and  belongs  to  this  class. 


S8J13J 

fcj  ■-  O-  fte  M 


jopu^g 


Bubbling  rales  are  due  to  fluid — serum,  mucus,  pus  or  blood  in  the 
bronchi.  When  the  fluid  is  thin,  we  get  a  bubbling  quality,  when  thick 
a  certain  sharpness  or  stickiness.  The  quality  depends  on  the  surround- 
ing lung  tissue.  In  consolidations  a  clear,  ringing  quality  is  noted. 
Bubbling  rales  vary  in  size,  with  the  site  of  production,  and  with  the 
quantity  and  character  of  the  exudate. 


124 


THE    EXAMIXATIOX    OF    THE    LT/XGS 


Xo  phrenic 
wave. 


Expansion 
+  .  v.  frem- 
itus +  .  v. 
resonance 
+  .   Percus- 
sion: 
hyper- 
resonant. 
Breath 
sounds: 
exagger- 
ated. 


'  V.  fremitus 
I  +  +,  v. 
|  resonance 
I  +,  Percus- 
{  sion:  slight 

dulness, 

Breath 

sounds: 

broncho- 
l  vesicular, 


Phrenic 
wave,-)-. 


Fig.  105. — Pyothorax.  Large  post-pneumonic  empyema.  The  whole  right  pleural 
cavity  was  filled  with  a  thick  purulent  exudate,  some  of  which  may  still  be  seen  adherent  to 
the  costal  pleura.  The  right  lung  is  complete^-  atelectatic,  and  has  been  compressed  into  a 
small  fibrous  mass.  The  heart  is  displaced  to  the  left,  and  the  diaphragm,  downward.  The 
left  lung  in  its  lateral  aspect  is  compressed  by  the  heart.  The  body  was  received  in  the  dis- 
secting room  from  the  Anatomical  Board,  the  clinical  diagnosis  having  been  "pneumonia." 


ADVENTITIOUS  BREATH  SOUNDS  125 

The  significance  of  rales  lies  mainly  in  their  (a)  quality  and  (b)  dis- 
tribution, as  indicating:  (1)  the  area  of  activity  of  the  pathologic  process; 
(2)  the  character  and  stage  of  the  lesion;  (3)  the  localization — in  the  lung 
or  pleura. 

The  primary  terms  crepitant,  crackling,  bubbling,  sibilant  and 
sonorous,  should  be  further  qualified  by  descriptive  adjectives  indicating 
their  size,  pitch,  number,  location  and  association  with  the  phases  of 
respiration,  e.g.,  "numerous,  fine,  high-pitched,  clear-cut,  metallic  rales 
heard  mainly  at  the  end  of  inspiration." 

Friction  Sounds. — These  are  also  spoken  of  as  friction  rales.  They 
may  be  heard  over  inflamed  serous  membranes  and  are  due  to  mechanical 
attrition  of  the  roughened  surfaces.  They  occur  in  the  pleura,  peri- 
cardium, and  rarely  peritoneum.  They  are  characteristically  described 
as  dry  and  leathery  (like  a  sound  produced  by  riding  on  a  new  saddle). 

They  differ  from  rales  in  that  they  tend  to  be  (1)  localized  fin  the  case 
of  pleuritis  to  the  axilla),  (2)  unilateral,  (3)  heard  both  with  in-  and  ex- 
piration. (4)  They  do  not  disappear  with  coughing,  (5)  they  are  in- 
creased by  pressure,  (6)  they  sound  close  to  the  ear,  (7)  they  are  attended 
by  pain  and  often  tenderness.  They  may  be  synchronous  with  the 
heart,  even  if  only  the  pleura  is  involved. 

It  is  by  no  means  always  possible  to  differentiate  between  an  intra- 
pulmonary  rale  and  a  pleuritic  friction,  but  the  following  points  often  aid 
in  arriving  at  a  correct  conclusion. 

Rales  Frictions 

(a)  Affected  by  coughing,  or  breathing,      (a)   Constant,  not    altered   by  coughing 

and  vary  spontaneously.  or  breathing. 

(6)   Sounds  are  often  "moist."  (6)   Sounds  are  more    "dry,"    leathery, 

creaking, 
(c)    Seem  more  distant.  (c)    Seem   closer  to  the  ear. 

{d)  Uninfluenced  by  pressure  on  the  chest     (d)  Increased  by  pressure,  accompanied 
wall.     Unaccompanied  by  local  pain.  by  pain,  which  is  also  increased  by 

pressure. 
(e)    Distribution     more     general,     more     (e)   Localized   in   extent,    generally   uni- 
widely    diffused.     Usually    bilateral.  lateral.     Most    common   in    axillary 

Commonly  heard  posteriori}'  or  near      >    .  region, 
bronchi. 
(J)    May  be  musical. '  (/)    Rarely  musical. 

(g)   Occur  in  showers,  are  uniform  in  size,     (g)   Size    and    character    of    component 

sound  elements  vary. 

Both  rales  and  frictions  may  be  closely  simulated  by  (1)  muscle 
sounds,  (2)  hair  on  the  chest. 

Method  of  Eliciting  Rales. — If  rales  are  suspected  to  be  present  but 
are  not  heard  in  the  course  of  ordinary  breathing,  the  patient  should  be 
asked  to  breathe  more  deeply;  or  to  cough,  and  afterward  breathe  deeply. 
The  crepitant  rales  of  early  tuberculosis  may  thus  be  elicited  (latent 
ralesj.  They  are  also  more  apt  to  be  heard  before  or  during  the  period 
of  the  morning  cough,  when  such  is  present.  Owing  to  the  faintness  of 
their  sound,  rales  are  only  rarely  heard  at  a  distance  from  the  seat  of 
their  origin,  although  it  is  said  that  the}'  are  occasionally  conducted  along 
the  ribs  and  may  even  be  heard  in  the  opposite  lung. 

Certain  tinkling,  gurgling  and  splashing  sounds  may  be  hoard  over 
the  chest,  especially  near  the  spinal  column,  as  the  result  of  liquid  passinu 
down  the  esophagus  when  the  patient  swallows.  These  sounds  are  often 
marked  and  delayed  in  the  presence  of  a  diverticulum. 


126 


THE    EXAMINATION    OF    THE    LUNGS 


Fig.  106. — Hydro-pneumothorax.  The  right  pleural  cavity  is  represented  as  partly 
filled  with  fluid,  partly  with  air.  The  rupture  of  the  lung  has  occurred  below  the  present 
fluid  level,  so  that  the  fistulous  tract  opens  into  the  effusion  and  bubbles  are  given  off  during 
respiration.  The  right  lung  is  collapsed.  The  left  lung  is  functionating  compensatorily 
despite  its  compression.  Succussion  splash  may  be  elicited  because  both  air  and  liquid  are 
present  in  a  large  cavity.  Metallic  tinkle  is  due  to  bubbles  from  the  fistulous  tract  passing 
up  through  the  effusion,  not  to  drops  of  liquid  falling  upon  the  surface  of  the  effusion. 


ADVENTITIOUS  BREATH  SOUNDS 


127 


Expansion 
— .     Vocal 
fremitus 
+  .     Vocal 
resonance 
+  •   Percus- 
sion: high 
pitched 
tympany, 
Breath 
sounds  :, 
broncho- 
vesicular 


Expansion 
— .     Inter- 
spaces full. 
Vocal 
fremitus  O. 
Vocal  reso- 
nance O- 
percussion 
dulness 
+  +  +. 
jBreath 
sounds  O- 
Phrenic 
shadow  O- 


[  Expansion 
'  +.     Vocal 
resonance 
+ .     Vocal 
fremitus  +. 
percussion 
:  hyper- 
resonant. 
Breath 
sounds': 
exagger- 
ated. 

Cardiac 
impulse 
and  left 
border 
displaced 
to  left. 


Fig.  107. — Large  Right-sided  Empyema.  The  diaphragm  is  flattened  and  depressed, 
forcing  the  liver  downward.  The  heart  is  pushed  to  the  left,  compressing  the  left  lung, 
which  is  contracted  and  exposes  the  heart  more  than  is  normally  the  case.  The  right  lung  is 
compressed  and  atelectatic,  and  in  part  adherent  to  the  chest  wall.  The  right  pleural 
cavity  contained  a  large  quantity  of  thick  purulent  exudate,  depressing  the  diaphragm  and 
liver  on  that  side.  On  the  left  side  the  diaphragm  is  pushed  upward  and  flattened  against 
the  chest  wall  by  the  colon.  Note  how  a  distended  stomach  or  colon  may  mechanically 
embarrass  the  heart.  This  has  an  important  bearing  upon  symptomatology  and  treatment 
in  cases  of  cardiac  decompensation  and  angina  pectoris.  {Specimen  the  property  of  Dr. 
T.  T.  Thomas.) 


128 


THE    EXAMINATION    OF    THE    LUNGS 


SUCCUSSION  SPLASH 


This  may  be  heard  on  ausculting  over  large  tense  chambers  which 
contain  both  liquid  and  air.  It  is  elicited  by  having  the  patient  cough, 
suddenly  move  the  body  from  side  to  side,  or  shake  his  chest. 

Succussion  splash  like  the  other  metallic  auscultatory  phenomena 
owes  this  quality  to  the  suddenness  with  which  the  liquid  is  thrown  into 
motion,  unrhythmic  vibrations  being  thus  originated.  For  its  production, 
a  stiff-walled  cavity  of  considerable  size  is  necessary.  It,  therefore, 
rarely  occurs  in  the  chest  except  in  hydro-pneumothorax.     Pulmonary 


Fig.  108-4.- 


-The  currently  accepted  but  erroneous  explanation  of  the  genesis  of 
metallic  tinkle. 


Fig.   1085. — The  true  mechanism  of  metallic  tinkle. 


cavities  are  generally  too  small,  too  flaccid  and  their  contents  too  viscid, 
to  produce  the  characteristic  sound.  It  may  be  simulated  by  imparting 
motion  to  the  liquid  in  an  atonic  stomach,  or  by  shaking  a  small  quantity 
of  water  in  a  bottle.  It  can  sometimes  be  heard  at  quite  a  distance  from 
the  patient,  especially  if  the  pneumothorax  communicates  with  a  bronchus 
and  the  mouth  be  open.     It  is  said  also  to  occur  over  very  large  pulmonary 


ADVENTITIOUS   BREATH    SOUNDS  129 

cavities.     It  never  occurs  in  simple  serous  or  purulent  effusion,  as  no  air 
is  present. 

Succussion  splash  and  metallic  tinkle  are  the  most  pathognomonic 
signs  of  hydro-pneumothorax,  but  they  only  occur  in  about  30  or  40 
per  cent,  of  the  cases  (Cruice). 

METALLIC  TINKLE 

This  is  a  clear,  vibrant,  musical  sound  which  may  be  heard  in  many 
cases  of  hydro-pneumothorax.  It  has  been  likened  to  the  distant  tinkling 
of  a  clear,  high-pitched  silver  bell. 

The  genesis  of  metallic  tinkle  may  be  illustrated  by  the  following  ex- 
periment (Fig.  108).  If  we  attach  a  stethoscopic  tubing  to  the  mouth 
piece  of  a  wash  bottle  and  listen  while  air  is  being  forced  through  the 
other  glass  tube  into  the  liquid,  the  phenomenon  of  metallic  tinkle  can 
be  accurately  reproduced.  It  will  further  be  noted  that  the  sound  occurs 
at  the  moment  the  bubble  is  given  off  and  not  at  the  time  at  which  it 
reaches  the  surface.  If,  on  the  other  hand,,  we  listen  while  water  is 
allowed  to  fall  from  a  pipette  upon  the  surface  of  the  water  only  a  dull, 
indifferent  sound  will  be  heard.1 

It  is  evident  both  from  this  and  for  anatomic  reasons,  that  metallic 
tinkle  is  due  to  air  bubbles  ascending  through  an  effusion  from  a  fistulous 
tract  in  the  lung  below  the  level  of  the  liquid,  and  not,  as  was  formerly 
taught,  to  liquid  dropping  from  a  moist  pleura  upon  the  effusion  beneath. 

Metallic  tinkle  may  also  be  produced  by  the  bursting  of  bubbles  in 
a  bronchial  tube  which  communicates  with  a  pneumothorax  or  by  a  bub- 
ble in  the  surface  of  a  moist  perforated  lung  above  the  level  of  the  fluid 
if  the  bubble  is  expelled  with  sufficient  force.  In  either  case  the  musical 
quality  is  due  to  the  rhythmic  vibration  of  the  air,  and  the  reverberation 
is  due  to  the  large  air-filled,  stiff-walled  resonator — the  pleural  cavitv 
(Fig.  106). 

1  Barach:  Arch.  Diag.,  January,  1910. 


CHAPTER  XI 
THE  VOICE  SOUNDS 

The  voice  sounds  consist  of: 

1.  Vocal  resonance :  the  voice  sounds  heard  upon  the  chest. 

2.  Bronchophony  :  increased  vocal  resonance. 

3.  Pectoriloquy:  bronchophony  with  articulated  overtones — syllabic 
speech.     "Whispered  pectoriloquy. 

4.  Egophony:  a  variety  of  bronchophony  having  a  nasal  or  bleating 
quality. 

These  signs  are  elicited  by  ausculting  over  different  areas  of  the  chest 
wall,  while  the  patient  speaks  or  whispers.  In  the  former  case  the  patient 
should  be  told  to  slowly  and  loudly  pronounce,  "one — one — one,"  or 
"ninety-nine"  in  the  lowest  range  of  his  natural  speaking  voice.  The 
examiner  should  note  any  differences  in  clearness  or  intensity  which  may 
exist  over  symmetrical  areas  of  the  thorax. 

VOCAL  RESONANCE 

The  vibrations  produced  in  the  larynx  during  phonation  are  increased 
in  intensity  (larger  wave  amplitude)  by  (l)'the  thorax  and  to  a  minor 
degree  by  the  trachea  and  bronchi,  (2)  by  the  air  chambers  above  the 
vocal  cords — the  mouth  and  nares.  These  structures  act  as  resonators, 
sympathetic  vibrations  being  set  up  in  them.  But  inasmuch  as  resona- 
tors act  selectively,  amplifying  only  certain  wave  lengths,  the  original 
sound  as  produced  in  the  larynx  undergoes  certain  changes  not  only,  in 
intensity  but  also  in  quality  and  pitch.  This  ex-plains  why  whispered 
pectoriloquy  may  be  heard  when  vocal  resonance  is  actually  diminished. 
Under  normal  conditions  the  vocal  sounds  heard  over  the  chest  are  much 
less  loud  and  clear  than  when  we  listen  over  the  larynx.  They  seem  dis- 
tant and  diffused,  are  lower  in  pitch,  and  the  distinct  articulations  of  the 
trachea  are  replaced  by  indistinct,  rumbling  sounds.  The  spoken  word 
is  lower  in  pitch  when  heard  through  the  chest  than  when  heard  at  the 
mouth,  owing  to  the  fact  that  the  lung  (resonator)  which  is  large,  rein- 
forces the  lower  notes.  When,  however,  the  lung  is  consolidated,  the 
sounds  heard  through  the  chest  wall  seem  higher-pitched  than  at  the 
mouth  because  the  pulmonary  tissue  being  infiltrated,  only  the  bronchi  re- 
main to  act  as  resonators,  and  also  being  small  in  size,  only  the  higher  notes 
are  amplified  (Mueller).  It  is  thus  evident  that  vocal  resonance  is  due 
to  somewhat  the  same  causes,  and  is  governed  by  the  same  laws  as  the 
breath  sounds.  Vocal  resonance  and  vocal  fremitus  have  the  same  origin. 
They  generally  vary  in  the  same  direction  and  in  the  same  proportions. 
Discrepancies  between  the  two  methods  of  examination  maybe  due  to  the 
fact  that  the  ear  perceives  vibrations  better  when  they  are  rapid,  the 
hand  when  they  are  slow.  Vocal  resonance  may  be  (1)  increased — more 
intense  and  clearer;  (2)  decreased — less  intense  and  muffled.     Here  clear- 

130 


THE   VOICE    SOUNDS  131 

ness  is  used  in  a  double  sense:  (a)  in  regard  to  the  fundamental  note — 
the  amount  of  sonorous  laryngeal  character;  or  (b)  in  regard  to  the  articu- 
lated overtones — syllabic  speech.  These  two  qualities — clearness  and 
loudness — do  not  necessarily  run  parallel,  they  may  be  diametrically 
opposed. 

Normal  Vocal  Resonance. — Vocal  resonance  is  normally  most  in- 
tense over  those  areas  of  the  chest  over  which  broncho-vesicular  breath- 
ing is  normally  heard — the  interscapular  region,  the  upper  sternum  and 
the  supraclavicular  apices.  But  even  here  no  distinct  articulate  speech 
can  be  appreciated;  only  an  indistinct  humming,  buzzing,  fluttering 
sound  not  unlike  that  of  a  voice  heard  at  the  distant  end  of  along  hall. 
The  sounds  of  both  the  spoken  and  the  whispered  voice  are  normally 
more  intense  on  the  right  side,  especially  over  the  upper  lobe,  both  an- 
teriorly and  posteriorly.  This  is  due  to  the  fact  that  the  right  pulmonary 
apex  lies  in  direct  contact  with  the  trachea,  and  also  because  the  right 
bronchus  is  almost  a  direct  continuation  of  the  trachea  which  points 
to  the  right  (Fetterolf)  (see  Figs.  75,  95,  103). 

In  women  vocal  resonance  is  feeble  because  the  fundamental  note  of 
the  larynx  does  not  stand  in  a  favorable  relationship  with  the  thorax — 
the  resonator.  (Small  tuning  forks  require  small  resonators.)  In  men 
the  relationship  is  generally  more  favorable,  although  even  here  we  meet 
with  great  degrees  of  difference.  In  singing  an  ascending  scale  from  one's 
lowest  base  to  one's  highest  treble,  both  vocal  fremitus  and  resonance 
will  become  progressively  less  intense,  and  at  a  given  point  disappear 
entirely.  Children  often  have  a  more  intense  fremitus  than  women  be- 
cause the  aforesaid  relationship  is  more  favorable,  although  as  a  rule 
vocal  fremitus  and  resonance  are  in  small  children  determined  with 
difficulty  (see  p.  140).  For  the  same  reason  these  signs  may  vary  with 
the  degree  of  inspiration  or  expiration  at  which  the  patient  speaks.  If 
the  sounds  heard,  remain  intense  even  with  marked  stethoscopic  pressure 
■ — which  tends  to  blot  out  the  sympathetic  vibrations  of  the  chest — we 
have  even  greater  reason  for  believing  that  loss  of  elasticity  and  infiltra- 
tion of  the  lungs  has  occurred  (Sewall). 

Vocal  resonance  may  be  diminished  or  absent  in  conditions  which 
interfere  abnormally  with  the  conduction  of  vibrations  from  the  larynx 
to  the  chest  wall,  such  as  obstruction  of  a  bronchus,  pleural  effusions, 
edema  or  the  chest  wall  or  excessive  subcutaneous  fat.  These  conditions 
act  through  their  effects  of  diffusion,  reflection  and  resonance  (see  p.  59). 

Vocal  resonance  is  generally  diminished  over  pleural  effusions  because 
vibrations  are  not  readily  transmitted  from  an  air-bearing  lung  to  the 
effusion.  //,  however,  the  lower  part  of  the  lung  which  is  in  contact  with 
the  effusion,  is  solidified,  either  as  the  residt  of  infiltration  or  compression, 
vocal  resonance  (as  well  as  fremitus  and  breath  sounds)  will  be  intensely 
transmitted  to  the  chest  wall. 

Vocal  resonance  may  be  diminished  in  some  rare  cases  of  pulmonary 
fibrosis  which  would  appear  contradictory  to  what  has  been  stated  re- 
garding normal  and  abnormal  sound  transmission,  since  solid  lung,  solid 
pleura  and  bronchus  have  relatively  the  same  density  and  we  should, 
therefore,  expect  what  we  usually  find — increased  voice  and  breath  sounds. 
Montgomery  suggests  that  diminished  sounds  may  be  due  to  (1)  "heavy 
strands  of  fibrous  tissue  alternating  with  air-bearing  lung  or  small  cavi- 
ties" thus  offering  a  "break"  in  transmission;  or  (2)  the  fact  that  the 


132  THE    EXAMINATION    OF    THE    LUNGS 

bronchi  are.  further  removed  from  the  chest  wall  by  the  thickened  pleura 
and  obliterated  peripherally,  or  that  their  lumen  is  actually  diminished. 
Vocal  resonance  may,  however,  be  diminished  in  some  uncomplicated 
cases  of  pulmonary  consolidation:  (1)  Owing  to  bronchial  obstruction 
due  to  (a)  secretion  (mucus,  pus,  blood,  serum),  (b)  to  pressure  from  with- 
out or  (c)'  a  malignant  growth  from  within.  In  the  first  instance,  es- 
pecially, the-  phenomenon  may  be  temporarily  dissipated  by  coughing 
or  deep  breathing.  (2)  Cases  not  explainable  upon  this  basis  may  be  due 
to  the  variable  effects  of  resonance  or  wave  interference  already  referred 
to  (p.  54)  (Montgomery). 

BRONCHOPHONY 

By  this  term  we  understand  vocal  resonance  increased  in  intensity 
and  clearness.  Over  normal  pulmonary  tissue  the  voice  sounds  are  even 
more  muffled  and  indistinct  than  when  we  listen  near  a  primary  bron- 
chus. If  the  lung  tissue  is  pathologically  altered  so  that  it  becomes  a 
better  conductor  of  sound  than  is  normally  the  case,  we  hear  an  increased 
vocal  resonance — bronchophony. l  In  other  words,  the  sounds  are  louder, 
higher-pitched,  clearer  and  more  amphoric  than  those  we  expect  to  hear 
in  the  locality  in  question,  or  than  those  we  clo  hear  in  the  corresponding 
area  of  the  opposite  (healthy)  side. 

Bronchophony,  therefore,  occurs  in:  (1)  Pulmonary  solidification — 
pneumonia,  tuberculosis,  atelectasis,  compression,  glandular  enlarge- 
ment especially  with  these  conditions  exists  near  to  a  large  bronchus, 
etc.  (2)  Pulmonary  cavitation — tuberculosis,  abscess,  gangrene,  etc. 
In  the  latter  instance  the  existence  of  bronchophony  is  in  part  due  to  the 
consolidation  which  accompanies  and  often  surrounds  the  cavities. 
Bronchophony  is,  therefore,  generally  encountered  in  association  with 
increased  vocal  fremitus,  bronchial  breathing,  percussion  dulness  and  ■metallic 
or  consonating  rales. 

PECTORILOQUY 

Pectoriloquy  is  exaggerated  bronchophony.  It  is  an  increased  vocal 
resonance  .in  which  syllabic  speech  (the  articulated  overtones)  can  be 
more  or  less  distinctly  recognized.  In  the  ordinary  speaking  voice,  as 
heard  through  the  chest  wall,  the  syllables  tend  to  be  drowned  out  by  the 
more  intense  and  lower-pitched  rumble  of  the  vowel  sounds,  hence  pec- 
toriloquy can  be  better  determined  during  the  act  of  whispering. 

The  Whispered  Voice  Sounds. — Whispering  is  the  result  of  articulate 
speech  in  which  the  glottis  plays  no  part.  Over  the  normal  chest  the 
whispered  voice  is  scarcely  audible,  since  whispering  does  not  set  up 
sympathetic  vibrations  of  the  thoracic  wall.  Over  areas  near  to  the 
primary  bronchi  one  hears  an  indistinct  swishing  sound.  The  transmis- 
sion of  syllabic  speech — whispered  pectoriloquy — is  pathologic. 

Our  judgment  must  be  based  not  on  the  loudness  but  on  the  dis- 
tinctness of  syllables.     The  actual  recognition  of  individual  syllables  is 

1  Bronchophony  as  the  derivation  of  the  word  implies,  suggests  the  emanation  of 
a  sound  from  the  bronchus.  We  receive,  the  impression  that  the  source  of  the  sound 
is  very  near  to  the  end  of  the  stethoscope,  or  as  if  someone  were  talking  directly  into 
the  latter.  Some  authorities  speak  of  a  "normal"  and  a  "pathologic"  bronchophony, 
using  the  former  term  as  synonymous  with  vocal  resonance. 


THE   VOICE    SOUNDS 


133 


Fig.  109. — Hydrothorax.  The  lung,  which  is  atelectatic,  is  surrounded  by  serum  which 
being  frozen  appears  as  ice  crystals.  The  dome  of  the  diaphragm  is  flattened  and  beneath  it 
are  seen  a  filled  stomach  and  a  portion  of  the  left  lobe  of  the  liver. 


134 


THE    EXAMINATION    OF    THE    LUNGS 


K\)l 


ffML- 


Fig.  110. — Sagittal  section,  viewed  from  the  left,  of  the  body  of  a  new-born  child,  the 
plane  of  section  being  2  cm.  to  the  right  of  the  midsternal  line.  Owing  to  adhesions  the 
horizontal  fissure  is  not  shown.  L,  liver;  R.M.L.,  middle  lobe  of  right  lung;  R.U.L.,  upper 
lobe  of  right  lung;  O.F.,  oblique  fissure;  R.L.L.,  lower  lobe  of  right  lung.  (Fetterolf  and 
Git  tings.) 


THE   VOICE    SOUNDS  135 

not  a  sine  qua  non.  Distinctness  is  rarely  sufficiently  clear  to  enable  us 
to  recognize  every  individual  word. 

The  whispered  voice  is  elicited  by  ausculting  the  chest  while  the 
patient  whispers  such  words  as  "one,"  "two,"  "three,"  "sixty-six." 
Over  the  lung  tissue  soft,  indistinct  sounds  are  heard.1  We  hear  "a 
feeble,  low-pitched,  blowing  sound,  these  characters  corresponding  with 
those  of  the  expiratory  sound  in  forced  breathing"  (Flint).  Sometimes 
no  audible  sound  is  produced.  Near  to  areas  of  consolidation  over  which 
bronchial  breathing  is  heard,  the  sounds  become  more  distinct  so  that 
some  syllables  can  be  recognized,  and  over  cavities  or  consolidations  near 
a  bronchus  or  cavities  communicating  with  a  bronchus,  the  acoustic 
impression  is  often  nearly  that  of  a  person  whispering  directly  into  the 
stethoscope.  In  women  and  children  the  voice  is  higher-pitched  and  in 
the  latter  the  large  bronchi  are  nearer  to  the  chest  wall,  thus  the  whispered 
voice  is  often  more  intense  than  in  men.  Whispered  pectoriloquy  is  an 
important  sign  of  pulmonary  consolidation  or  cavitation.  What  has 
already  been  stated  in  regard  to  vocal  resonance  and  bronchial  breathing 
applies  to  it.  It  is  much  less  taxing  to  the  patient  than  speaking,  and  is 
often  a  useful  method  of  determining  pulmonary  infiltration  if  a  patient 
breathes  so  badly  that  bronchial  breathing  cannot  be  elicited.  Whispered 
pectoriloquy  is  sometimes  more  distinct  than  spoken  bronchophony, 
and  may  be  elicited  when  the  latter  is  absent,  owing  to  the  resonating 
properties  of  the  tissues. 

The  whispered  voice  test  further  has  the  advantage  over  that  of  the 
spoken  voice  that  does  not  set  up  sympathetic  vibrations  in  the  chest  wall 
(resonator)  and  that  an  increase  in  intensity,  therefore,  speaks  more 
strongly  in  favor  of  actual  change  in  the  pulmonary  tissue. 

The  whispered  voice  is  normally  heard  most  clearly  from  the  right  apex 
to  the  second  intercostal  space.  Posteriorly  it  is  less  intense  and  never 
extends  below  the  scapular  spine.  On  the  left  side  its  intensity  is  much 
less  and  its  extent  much  more  limited. 

EGOPHONY 

Egophony  is  a  modified  bronchophony  characterized  by  a  tremulous, 
high-pitched,  bleating  quality.  It  has  been  compared  to  the  bleating 
of  a  goat,  the  speech  of  a  person  with  a  cleft  palate,  or  to  the  voice  of  a 
ventriloquist.  It  may  be  imitated  by  attempting  to  throw  the  voice 
through  the  nares,  while  speaking  with  the  nostrils  occluded,2  or  by  the 
interposition  of  a  thin  cork  between  the  larynx  and  the  stethoscope. 
It  may  be  heard  just  below  the  upper  level  of  pleural  effusions  while  the 
patient  is  being  examined  for  vocal  resonance,  and  when  present  is  a 
valuable  sign  of  pleural  exudation.  It  is  perhaps  clue  to  the  abnormal 
relationship  between  the  bronchi  (which  become  shorter  when  the  lung  is 
collapsed)  and  the  compressed  lung  in  pleural  effusions  that  the  necessary 
physical  conditions  are  brought  about  which  will  reinforce  the  high- 
pitched  nasal  sounds. 

1  Some  people  have  never  learned  to  whisper,  some  whisper  during  inspiration, 
which  greatly  modifies  the  sounds  produced. 

2  Egophony  was  formerly  attributed  to  (a)  flattening  of  non-cartilaginous  bronchi 
by  pressure  of  the  effusion,  so  that  they  acted  like  reeds  (Laennec);  (6)  vibrations  of 
the  walls  of  small  bronchi  by  actual  collision — interruption  of  the  air  current  ( Wint  rich ) ; 
(c)  the  articulation  of  overtones — only  the  higher  harmonics  passing  through  the  effu- 
sion (Stone);  (d)  to  vibrations  passing  through  a  thin  layer  of  fluid. 


CHAPTER  XII 
THE  PHYSICAL  FINDINGS  IN  INFANTS  AND  YOUNG  CHILDREN1 

NORMAL  CONDITIONS 

Chest  Inspection. — The  anteroposterior  diameter  is  relatively  in- 
creased in  infants  (under  two  years) .  The  sternum  is  prominent  and  the 
ribs  more  horizontal.  Breathing  is  of  the  abdominal  type  for  the  first 
five  or  six  years  or  even  longer  (see  Fig.  17).  The  chest  wall  is  thin  and 
resilient  and  readily  transmits  sound  vibrations.  Auscultation  should 
be  practised  before  palpation  or  percussion,  lest  crying  interfere  with  the 
former. 


Fig.  111. — Body  of  a  new-born  child  from  which  the  median  portion  of  the  anterior  chest 
wall  has  been  removed.  R.L.,  right  lung;  R.T.,  right  lobeof  thymus;  R. J. V.,  right  internal 
jugular  vein;  R.C.A.,  right  common  carotid  artery;  T,  trachea;  L.C.A.,  left  common  carotid 
artery  ;L.  J.  V.,  left  internal  jugular  vein;  L.T.,  left  lobe  of  thymus;  L.L.,  left  lung;  P,  pericar- 
dium.     (Fetterolf  and  Gittings.) 

Palpation. — Expansion  is  slight  and  vocal  resonance  less  marked  than 
in  adults  (see  vocal  resonance).  The  apex  beat  is  in  the  fourth  interspace, 
just  within  or  even  to  the  left  of  the  left  mid-clavicular  line. 

Percussion. — Percussion  must  be  extremely  light — finger  percussion  is 
often  necessary.     If  a  forcible  stroke  be  employed  the  whole  lung  as  well 

1  For  assistance  in  the  preparation  of  the  following  paragraphs,  we  are  indebted  to 
Dr.  J.  C.  Gittings. 

136 


PHYSICAL    FINDINGS    IN    INFANTS    AND    YOUNG    CHILDREN  137 

as  the  neighboring  abdominal  viscera  will  be  thrown  into  vibration  and 
topographic  percussion  will  become  impossible.  The  child  must  .be 
placedfin  the  sitting  or  standing  position — or  prone  or  supine — never  on 
one  side.  Owing  to  the  flexibility  of  the  thoracic  cage  the  lowermost 
lung  when  the  infant  lies  upon  one  side  becomes  compressed  and  yields  a 
less  resonant  note.  The  posterior  portion  of  the  thorax  should  be  ex- 
amined while  the  infant  held  in  the  nurse's  arms,  looks  backward  over 
her  shoulder.  The  general  percussion  note  is  resonant,  sometimes  hyper- 
resonant  (higher  pitched  than  in  adults)  from  the  clavicle  to  the  fourth 


Fig.  112. — Thymus  in  situ.  The  anterior  pulmonary  margins  are  pushed  aside.  The 
lower  border  of  the  thymus  gland  overlies  the  greater  portion  of  the  heart.  (After  Fetterolf 
and  Gittings.) 

rib  on  right  side  anteriorly;  to  eighth  rib  posteriorly  (on  account  of  high 
dome  of  liver).  Below  these  levels  the  note  shades  into  liver  dulness  at 
the  sixth  and  tenth  ribs,  respectively. 

In  the  axilla  and  posteriorly  on  the  left  side  gastric  tympany  may 
affect  the  normal  note,  as  high  as  the  sixth  rib.  This  tympanitic  quality 
may  sometimes  be  eliminated  or  at  least  diminished  by  the  method  of 
lateral  limitation — three  fingers  down,  percuss  the  middle  one. 

On  the  left  sidebelow  the  inner  third  of  the  clavicle  the  note  is  impaired 
or  dull,  shading  into  the  area  of  cardiac  dulness  (Hamill),  owing  to  poor 
expansion  of  left  apex  over  the  great  vessels,  possibly  in  part  to  left  lobe 
of  thymus.  Crying  produces  a  rigid  chest  and  may  cause  dulness  over 
the  lower   lobes.     Percussion   during   crying   may    yield  a  cracked-pot 


138 


THE    EXAMINATION    OF    THE    LUNGS 


sound.  Percussion  is  generally  less  satisfactory  than  auscultation.  The 
sense  of  resistance  is  often  a  valuable  criterion  in  deciding  between  con- 
solidation and  liquid  effusion. 

The  heart  is  large,  lies  higher  in  the  thorax,  as  well  as  more  horizon- 
tally. Cardiac  dulness,  therefore,  normally  extends  relatively  further  to 
the  left  than  in  adults.  It  may  normally  extend  }/±  inch  beyond  the  mid- 
clavicular line.  Dulness  due  to  the  right  auricle,  however,  rarely  extends 
beyond  the  sternal  line.  The  great  vessels  are  relatively  large.  This, 
together  with  the  possibility  of  a  persistent  thymus  gland  renders  a 
determination  of  the  upper  border  difficult.  This  difficulty  is  further 
enhanced  by  the  normal  dull  area  at  the  inner  third  of  the  left  clavicle 
already  alluded  to. 


A>A     T|B 


Fig.  113. — Horizontal  section,  viewed  from  beneath.  Body  of  a  new-born  child  at  the 
level  of  the  upper  border  of  the  third  rib.  E.,  esophagus;  V.A.M.,  vena  azygos  major; 
R.L.,  right  lung;  R.B.,  right  bronchus;  R.P.A.,  right  pulmonary  artery;  S.V.C.,  superior 
vena  cava;  A. A.,  ascending  part  of  aortic  arch;  T.B.,  thymus  body ;  P. A.,  pulmonary  aorta; 
L.P.A.,  left  pulmonary  artery;  L.L.,  left  lung;  L.B.,  left  bronchus;  T.A.,  thoracic  aorta. 
(Fetterolf  and  Gittings.) 

During  the  first  year  the  apex  beat  is  usually  found  in  the  fourth 
intercostal  space.  This  may  be  so  until  the  thirteenth  year,  after  which 
in  normal  children,  it  is  always  in  the  fifth  interspace.  As  in  adults,  the 
existence  of  cardiac  hypertrophy  can  usually  be  satisfactorily  determined 
by  inspection  and  palpation  alone.  If  the  left  ventricle  is  chiefly  in- 
volved, a  heaving  systolic  thrust  is  felt  outside  of  the  mid-clavicular  line. 
In  case  the  right  ventricle  is  chiefly  affected,  the  thrust  is  diastolic  in  time 
and  most  marked  in  the  epigastrium  because  the  right  ventricle  retracts 
from  the  chest  wall  to  rebound  in  diastole  (Talley).  Since  compensatory 
and  reparative  changes  in  youth  are  good,  marked  degrees  of  cardiac 
hypertrophy  are  often  seen  in  children  with  valvular  lesions  (Figs.  15, 122). 


PHYSICAL    FINDINGS    IN    INFANTS    AND    YOUNG    CHILDREN 


139 


Cardiac  Arrhythmia. — Sinus  arrhythmia,  or  juvenile  arrhythmia  as  it  is 
often  called,  is  as  the  latter  name  implies,  very  common  in  infants  and 
children,  especially  in  high  strung  youngsters  and  following  infections 
(see  p.  169). 

Extrasy stoles  are  also  common,  more  so  indeed  in  children  with  ap- 
parently normal  hearts  than  in  those  with  definite  valvular  lesions. 
Tachycardia  is  frequent  after  five  years  of  age  and  bradycardia  may  occur 
during  convalescence  from  fevers  and  in  association  with  jaundice. 

Auricular  fibrillation  is  rarely  met  with  and  when  encountered  is 
usually  only  noted  in  fatal  cases  of  diphtheria  or  rheumatic  pancarditis. 


Fig.  114. — Horizontal  section  of  a  new-born  infant's  thorax  at  the  upper  level  of  the 
ensiform  cartilage:  showing  its  cylindrical  shape.  L.L.,  left  lung;  P. A.,  pulmonary  aorta; 
L.T.,  left  lobe,  and  R.T.,  right  lobe  of  thymus  body;  A. A.,  ascending  part  of  aortic  arch; 
S.V.C.,  superior  vena  cava;  R.L.,  right  lung;  B.T.,  bifurcation  of  trachea;  E.,  esophagus; 
A.,  descending  part  of  aortic  arch.     {After  Fetter olf  and  Gittings.) 


Auricular  flutter  is  even  more  unusual,  although  Ritchie  has  reported  two 
cases  in  children  under  ten  years.  Heart  block  also  has  been  observed  in 
association  with  diphtheria. 

The  prognostic  significance  of  arrhythmia  in  children  is  essentially 
the  same  as  in  adults.1 

Auscultation. — Respiration  in  infants  and  young  children  is  irregular 
in  rhythm  and  very  irregular  in  depth.  (Respiration  being  entirely  a 
postnatal  function,  development  of  this  function  is  relatively  retarded. 
It  does  not  become  fully  developed  until  the  child  has  become  active  upon 

1  For  more  detailed  information  see  Talley,  J.  E. :  "The  Physical  Examination 
of  the  Heart  in  Children."  Arch.  Pediatrics,  September,  1915,  to  which  article  I  am 
indebted  for  some  of  the  foregoing  facts. 


140  THE    EXAMINATION    OF    THE    LUNGS 

its  feet.  This  earty  irregularity  of  breathing  accounts  in  great  part  for 
the  difficulty  in  interpreting  the  auscultatory  phenomena.) 

In  early  life,  the  breath  sounds  are  relatively  harsh,  and  loud.  Expira- 
tion is  clearly  heard,  and  in  comparison  with  an  adult  relatively  pro- 
longed. Exaggerated  or  vesiculo-bronchial  breathing  is,  therefore,  a 
normal  finding  (puerile  breathing). 

The  areas  overlying  the  bifurcation  of  the  bronchi  anteriorly  extend- 
ing 1  to  3  cm.  to  the  right  of  the  sternal  margin,  and  1  to  2  cm.  to  the  left 


Fig.  115. — The  infant's  chest  is  circular  in  outline.  The  abdominal  viscera  are  large. 
The  proximity  of  the  stomach  and  colon  to  the  lower  portion  of  the  lungs  imparts  a  tympan- 
itic quality  to  the  lower  lobes,  especially  the  left,  and  renders  very  light  percussion  essential. 
The  heart  lies  almost  horizontally,  hence  cardiac  dulness  extends  relatively  further  to  the 
left  than  is  the  case  in  adults.    It  also  lies  about  one  interspace  higher  in  infants. 

(at  level  of  the  first  interspace  and  the  second  rib)  yield  broncho-vesicular 
breathing.  Posteriorly  this  is  also  found,  especially  on  the  right  side. 
Vocal  resonance  in  young  children  is  hard  to  elicit  as  child  cannot  be  con- 
trolled. Whispered  pectoriloquy  can  often  be  heard,  normally,  over  the 
areas  of  broncho-vesicular  breathing. 

Owing  to  tardy  development  of  the  accessory  muscles  of  respiration 
and  of  the  laryngeal  and  pharyngeal  muscles,  a  slight  hypersecretion  of 


PHYSICAL    FINDINGS    IN    INFANTS    AND    YOUNG    CHILDREN  141 

mucus  in  the  pharynx,  naso-pharynx  or  larynx,  often  produces  coarse 
moist  rales  which  may  be  heard  all  over  chest.  The  heart  sounds  tend  to  be 
embryocardial  in  character,  the  first  sound  having  a  valvular  quality, 
and  the  diastolic  pause  being  brief.  The  pulmonic  second  sound  is 
loud  and  more  intense  than  the  aortic  (retracted  lungs,  more  superficial 
position).     Heart  sounds  and  murmurs  are  loud. 


Fig.  116. — Horizontal  section  of  an  infant  thorax  showing  its  cylindrical  contour  as 
well  as  the  relatively  large  size  and  horizontal  position  of  the  heart.  L.  =  left  ventricle 
R.  =  right  ventricle. 

PATHOLOGIC  CONDITIONS 

Small  serous  effusions  in  the  pleural  cavities  usually,  but  not  in- 
variably, produce  a  dull  note  on  percussion.  Large  serous  effusions  may 
produce  a  dull  or  even  a  flat  sound,  as  in  adults,  but  quite  often,  a  slightly 
tympanitic  note  results,  due  to  relaxation  of  pulmonary  tension  and  to 
abdominal  tympany.  The  note  over  empyemas  is  more  apt  to  be  dull 
or  fiat,  but,  for  the  same  reasons,  this  is  not  invariable.  In  serous  or 
purulent  effusions  as  a  general  rule,  therefore,  we  do  not  find  as  flat  a 
note  as  in  adults,  under  the  same  conditions. 

In  ausculting  over  a  pleural  effusion  (serum  or  pus)  the  breath  sounds 
often  persist  and  in  some  cases  the  diagnosis  can  be  definitely  established 
only  by  the  exploring  needle.  In  the  case  of  large  effusions,  especially  if 
purulent  and  causing  marked  compression  of  lungs,  we  may  find  bronchial 
or  cavernous  breathing,  with  whispered  pectoriloquy,  from  the  clavicle 
down  as  far  as  the  third  or  even  the  fourth  rib.  An  erroneous  diagnosis' 
of  cavity  is  sometimes  made.     Cavities  in  children  are  rare. 

The  second  pulmonic  sound  is  actually  and  relatively  louder  than  the 
second  aortic — this  difference  persisting  throughout  childhood.     Organic 


142 


THE    EXAMINATION    OF    THE    LUNGS 


LSA 


AA 


LB 


uAL 


LAA 


LA 


X 


MV 


X 


Fig.  117. — Sagittal  section  of  the  body  of  a  newly  born  child  viewed  from  the  right,  the 
plane  of  the  section  being  0.25  cm.  to  the  left  of  the  mid-sternal  line.  M.V.,  mitral  valve; 
L.A.,  left  auricle;  L.A.A.,  left  auricular  appendage;  L.V.P.,  orifices  of  the  left  pulmonary 
veins;  R.P.A.,  right  pulmonary  artery;  L.B.,  left  bronchus;  L.S.A.,  left  subclavian  artery; 
I. A.,  innominate  artery;  L.C.A.,  left  common  carotid  artery;  L.I.V.,  left  innominate  vein; 
A. A.,  aortic  arch;  A.L.,  aortic  leaflets;  T.L., tricuspid  leaflets;  R.V.,  right  ventricle;  D,  dia- 
phragm; L,  liver. 


PHYSICAL    FINDINGS    IN    INFANTS    AND    YOUNG    CHILDREN 


143 


A 


Fig.   118.— Sagittal  section  of   the  body  of   a  newly    born  infant,  viewed  from  the  left 
The  plane  of  section  being  0.75  cm.  to  the  left  of  the  mid-sternal  lum     i 
auricle;  R. A. a 
artery;  L.I.V. 
L.B.,  left  bror 
inferior  pulmonary  vein;  T.A.,  thoracic  aorta. 


144  THE    EXAMINATION    OF    THE    LUNGS 

systolic  murmurs,  produced  at  the  mitral  orifice,  usually  can  be  heard 
clearly  all  over  the  area  of  the  heart  and  posteriorly,  on  the  left  side.  This 
is  true  to  a  lessened  extent  of  aortic  systolic  murmurs  in  double  aortic 
disease.  Aortic  diastolic  murmurs,  even  more  frequently  than  in  adults, 
are  heard  best  near  the  apex  or  at  the  fourth  left  costal  cartilage. 

Functional  murmurs  are  very  common  in  childhood  and  often  simulate 
organic  murmurs  in  quality,  but  are  heard  loudest  over  the  base  and  in  the 
reclining  position.  They  become  much  less  marked  when  the  child  sits 
up — an  important  distinction,  since  venous  hums  are  intensified  by  this 
procedure. 

Compression  of  the  left  lung  by  an  enlarged  heart  or  a  pericardial 
effusion  gives  the  signs  of  consolidation  posteriorly — dulness  and 
bronchial  breathing — and  must  be  differentiated  from  pneumonia. 

In  addition  to  the  minute  anatomic  relations  the  preceding  figures 
illustrate  the  following  facts: 

1.  The  large  amount  of  space  in  the  antero-posterior  direction  occu- 
pied bj'  the  heart,  enlargement  of  which  (dilatation,  pericardial  effusion) 
would  compress  the  upper  part  of  the  lower,  and  the  lower  part  of  the 
upper  pulmonary  lobes,  causing  bronchial  breathing  over  the  correspond- 
ing areas  of  the  chest. 

2.  The  superior  vena  cava  enters  the  auricle  at  a  plane  posterior  to 
that  of  the  inferior  cava,  so  that  the  blood  stream  from  the  latter  is 
directed  upward  by  the  Eustachian  valve  and  not  to  the  left  as  is 
commonly  stated. 

3.  The  tricuspid  orifice  is  practically  vertical,  not  horizontal,  and 
opens  toward  the  left  and  slightly  forward.  The  lower  part  of  the  right 
ventricle  is  so  near  the  level  of  the  right  auricle  that  gravity  can  play  but 
an  inconspicuous  part  in  the  filling  of  the  ventricle. 

4.  The  mitral  and  tricuspid  orifices  lie  in  planes  almost  at  right  angles 
to  each  other. 

5.  The  two  posterior  aortic  leaflets  are  attached  to  the  base  of  the 
mitral  leaflet  (see  Flint's  murmur). 

6.  The  mitral,  tricuspid  and  aortic  valves  are  practically  contiguous 
structures.  This  fact  together  with  the  actually  small  size  of  the  heart, 
and  the  thinness  of  the  chest  wall,  explains  why  sounds  produced  at  these 
areas  are  often  differentiated  with  difficulty.  A  systolic  aortic  murmur 
can  only  be  identified  with  certainty  if  heard  in  the  neck.1 

For  the  sake  of  conserving  time  in  the  recording  of  physical  signs 
various  systems  of  graphic  registration  have  been  suggested.  That 
which  follows  is  modified  after  Barach's  plan.  Unfortunately  no  uni- 
form system  has  thus  far  been  adopted  by  clinicians  (Fig.  119). 

If  rales  occur  during  inspiration  they  are  charted  before,  if  during 
expiration,  after  the  symbol  which  stands  for  the  type  of  breathing. 

PRACTICAL  CONSIDERATIONS 

In  examining  the  lungs,  the  chest  must  be  exposed  and  the  patient 
must  not  be  in  a  recumbent  position  if  the  greatest  possible  accuracy  is 
a  desideratum.  The  importance  of  inspection,  especially  in  chronic  pul- 
monary disease,  cannot  be  over-emphasized.  Symmetric  areas  of  the 
chest  must  be  examined  and  compared  step  by  step.  In  determining 
1  Fetterolf  and  Gittixgs:  Am.  Jour.  Dis.  Children,  I,  1911,  6. 


PHYSICAL    FINDINGS    IN    INFANTS    AND    YOUNG    CHILDREN- 


US 


fremitus  it  is  well  to  bear  in  mind  that  the  ulnar  nerve  distribution  is 
more  sensitive  than  the  radial  and  hence  the  hand  should  be  slightly 
rotated  toward  the  outer  side. 

In  practising  percussion  the  beginner  usually  employs  far  too  much 
force.  This  is  always  disagreeable  and  often  painful  to  the  patient;  it  is 
also  hard  on  the  examiner's  fingers.  As  a  general  rule,  the  more  experi- 
enced the  examiner  the  lighter  the  percussion  stroke  he  emploj-s.  Force 
and  accurate  limitation  are  not  compatible.  The  blow  must  be  delivered 
from  the  wrist  (not  the  arm),  it  must  fall  vertically  and  the  striking- 
finger  must  be  quickly  withdrawn.  Good  percussion  is,  and  should  be, 
a  "gentle  art. " 

Before  ausculting,  see  to  it  that  the  patient  breathes  properly.  Res- 
pirations should  be  a  trifle  deeper  than  is  normally  the  case  and  the  mouth 
slightly  open.  "Throaty"  sounds  must  be  eliminated  and  expiration 
must  be  purely  passive.     The  areas  over  which  the  breath  sounds  may 


Tympany: 

Hyper- re so nance: 


o 


Honnal   Breathing: 


Vfeak   breathing: 


Exaggerated  breathing: 


Broncho-vesicular  breathing: 


A 


Bronchial   breathing: 
Cavernous   breathing: 

Cog-wheel   breathing: 

Friction: 

Crepitant  rales: 

Crackling  rales: 

Bubbling  rales: 

Sibilant  or  sonorous  rales: 


/    \ 

•  \ 

N 


s/ 


Fig.  119. 

normally  be  somewhat  harsh,  must  be  borne  in  mind,  and  examination  of 
the  supraclavicular  and  suprascapular  portions  of  the  lung  as  well  as  the 
apex  of  the  axilla  must  not  be  omitted. 

A  diagnosis  of  incipient  tuberculosis  based  upon  a  single  examination 
is  always  a  questionable  procedure.  Repeated  examinations  and  fur- 
ther observation  are  usually  advisable.  In  really  early  pulmonary  tuber- 
culosis, abnormality  in  the  physical  signs  is  very  slight  and  may  be  absent. 
A  careful  consideration  of  the  patient's  history  and  an  observation  of  his 
temperature  and  pulse  are  often  more  reliable  than  slighl  abnormality 
of  his  physical  signs. 

The  physical  signs  of  pleural  effusion  and  pulmonary  consolidation 

are  variable,  and  the  classical  text-book  method  differentiation  often 

fallacious.     Consolidation  may  yield  absent  breath  sounds;  an  effusion, 

bronchial  breathing,  bronchophony  and  fremitus.     The  reasons  for  this 

10 


146 


THE    EXAMINATION    OF    THE    LUNGS 


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Fig.  120.— The  accomparrying  chart,  which  is  the  type  used  at  the  Phipps  Institute, 
depicts  the  physical  sisns  encountered  in  a  case  of  right-sided  pulmonary  tuberculosis  with 
cavitation  in  the  upper  lobe,  and  of  left-sided  pleural  effusion.  In  addition  to  iurmshing 
excellent  eraphic  records  the  details  of  which  can  be  grasped  at  a  glance,  the  method  is 
invaluable" for  students  since  they  are  required  to  describe  exactly  the  signs  occurring  in 
every  region  of  the  chest.  This  encourages  care  for  detail  and  eliminates  negative 
results.     Red  shading  indicates  tympany. 


PHYSICAL    FINDINGS    IN    INFANTS    AND    YOUNG    CHILDREN 


147 


variation  of  physical  signs  have  already  been  discussed.  The  exploring 
needle  should  be  unhesitatingly  employed  in  doubtful  cases.  Properly 
performed,  this  procedure  is  unattended  by  risk,  or  any  considerable 
degree  of  pain. 

The  explanation  of  abnormal  physical  signs  as  "thickened  pleura" 
should  be  made  only  as  a  last  resort.  In  this  condition  physical  signs 
are  slight  or  entirely  absent,  unless  the  lung  is  also  involved. 

With  obscure  pulmonary  symptoms,  especially  in  men  past  thirty-five 
years,  the  possibility  of  aortic  aneurism  must  ever  be  borne  in  mind, 
especially  if  associated  with  cough,  chest  pain,  or  dyspnea  for  which 
symptoms  no  evident  cause  can  be  demonstrated. 


Fig.  121. — The  graphic  signs  here  depicted  would  be  construed  as  follows:  Right  upper 
lobe:  high-pitched  tympany,  surrounded  by  dulness,  cavernous  breathing,  inspiratory  bub- 
bling rales.     Right  axilla:  friction  and  below  this  area  weak  breath  sounds. 

Left  upper  lobe:  slight  dulness,  broncho-vesicular  breathing,  subcrepitant  inspiratory 
and  crackling,  expiratory  rales.  Left  axilla:  cog-wheel  breathing,  below  this  area,  exaggerated 
breath  sounds. 

THE  X-RAY 

The  X-ray,  especially  as  a  fluoroscope,  has  become  a  useful  adjunct 
in  intrathoracic  diagnosis.  It  enables  us  to  "control"  our  percussion 
and  often  definitely  establishes  the  presence  or  absence  of  deep-seated 
mediastinal  lesions — aneurism,  lymphadenitis,  central  pneumonia,  tu- 
mors, foreign  bodies,  mediastinal  displacement,  pulmonary  abscess,  etc. 
— in  cases  in  which  ordinary  physical  diagnosis  only  permits  us  to  "sus- 
pect" the  lesion.  The  same  statement  applies  to  some  cases  of  localized 
pneumothorax  and  of  pulmonary  fibrosis  involving  the  diaphragmatic 
pleura,  as  well  as  to  small  pleural  effusions. 

On  the  other  hand,  the  ordinary  methods  of  diagnosis  are  far  superior 
to  the  X-ray  in  cases  of  incipient  or  early  pulmonary  tuberculosis  and  in 
congestion  of  the  lungs.  In  these  instances  the  mistakes  are  usually  on 
the  side  of  the  radiographer.  The  X-ray  is  rarely  of  much  use  as  an  early 
diagnostic  method  in  cardiac  or  pulmonary  disease. 


PART  II 
THE  EXAMINATON  OF  CIRCULATORY  SYSTEM 

By  George  W.  Norris,  A.  B.,  M.  D. 

CHAPTER  XIII 
THE  CIRCULATORY  SYSTEM 

INSPECTION 

The  most  important  signs  to  be  looked  for  are:  ctyspnea,  orthopnea, 
pallor,  flushing  or  cyanosis;  distention  or  pulsation  of  the  superficial 
arteries  or  veins,  especially  in  the  neck;  edema,  especially  of  the  dependent 
portions  of  the  body  and  of  the  face;  clubbing  of  the  fingers,  inequality 
of  the  pupils;  normal  or  abnormal  pulsations,  especially  of  cardiac  apex 
and  the  epigastrium;  distention  of  the  abdomen,  in  general,  in  the  hepatic 
region,  and  in  the  flanks. 

Orthopnea,  the  state  in  which  the  patient  has  to  sit  up  in  order  to  get 
his  breath — indicates  that  the  heart  is  drawing  on  its  last  reserves. 
Circulatory  pallor  is  seen  in  connection  with  low  blood-pressure  and  periph- 
eral anemia.  Flushing  of  the  face  may  be  seen  in  fevers,  excitement 
also  in  aortic  insufficiency  and  at  times  in  arterial  hypertension.  Cyano- 
sis indicates  insufficient  oxygenation  of  the  blood,  and  is  seen  chiefly  in 
mitral,  pulmonary  and  tricuspid  lesions  associated  with  pulmonary 
congestion.  It  is  most  marked  in  the  face,  hands,  and  feet.  Distention 
of  the  superficial  veins  indicates  high  venous  pressure,  generally  a  weak 
right  heart;  or  local  obstruction  to  the  venous  circulation  and  an  effort 
to  establish  collateral  circulation.  Circulatory  edema  occurs  character- 
istically at  the  end  of  the  day,  and  in  the  dependent  portions  of  the  body; 
renal  edema  occurs  in  the  morning  and  upon  the  face.  Clubbing  of  the 
fingers  indicates  long-standing  stasis  of  the  pulmonary  circulation — 
chronic  cardiac  or  pulmonary  disease.  Anisocoria — pupillary  inequality — 
may  result  from  pressure  of  a  thoracic  aneurism  upon  the  cervical  sym- 
pathetic. Pidsalion  of  the  cervical  vessels  may  be  arterial  or  venous.  In 
the  former  instance  it  may  be  due  to  marked  alternations  of  blood-pres- 
sure and  an  hypertrophied  heart,  or  to  a  local  aneurism.  Venous  pulsa- 
tions may  be  seen  in  the  jugular  veins  of  recumbent  subjects.  Normally 
three  small,  faint  waves  can  be  made  out.  These  are  stasis  waves;  they 
are  not  due  to  regurgitation  from  the  right  heart.  A  single  large  systolic 
pulsation  may  result  from  (a)  a  transmitted  impulse  from  a  contiguous 
artery,  (6)  tricuspid  insufficiency,  (c)  aneurismal  varix.  A  capillary 
pulse  (Quincke's  pulse)  consists  in  an  alternate  flushing  and  blanching 
of  a  finger  tip  when  slight  pressure  is  made  upon  the  lower  portion  of  the 

149 


150  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

finger  nail.     It  may  occur  in  cases  of  aortic  insufficiency.     It  is  not  an 
early  sign  and  is  elicited  with  difficulty. 

The  patient  who  suffers  from  mitral  and  tricuspid  disease  is  apt  to 
complain  of  orthopnea,   cough,   cyanosis,   and  hemoptysis    (pulmonary 


Fig.    122. — Stunted  growth  and  bulging  of  the  precordium  resulting  from  mitral  obstruction 
and  insufficiency  in  a  boy  of  fifteen  years. 

Pulmonary  valve  Aortic  valve 


Fig.   123. — Showing  partial  overlapping  of  the  aortic  and  pulmonic  valvular  orifices.     The 
pulmonic  is  the  most  superficial  of  all  the  cardiac  valves. 

stasis),  digestive  disturbances  (portal  congestion)  and  edema.  Aortic 
lesions  are  characteristically  associated  with  dyspnea  on  exertion,  vertigo, 
flushing,  palpitation,  precordial  oppression. 


THE    CIRCULATORY    SYSTEM 


151 


THE  HEART— ANATOMICAL  CONSIDERATIONS 

The  heart  lies  obliquely  placed  behind  the  lower  two-thirds  of  the 
sternum.  It  rests  upon  the  upper  surface  of  the  diaphragm,  two-thirds 
of  its  bulk  being  placed  to  the  left  of  the  mid-sternal  line.  The  base  ex- 
tends from  the  lower  border  of  the  second  left  costal  cartilage  to  the  upper 


.^5 


Fig.  124. — Normal,  position  of  the  heart.  A.  =  aorta;  P. A.  =  pulmonary  artery; 
R. A.  =  right  auricle;  S.C.  =  superior  vena  cava;  T.  =  trachea;  E.  —  esophagus;  S. A. .sub- 
clavian artery;  S.V.  =  subclavian  vein;  S.  =  spinal  cord;  C.   =  clavicle. 


border  of  the  third  right  costal  cartilage.  The  apex  lies  in  the  fifth  left 
intercostal  space,  about  8  cm.  to  the  left  of  the  mid-sternal  line.  The 
aorta  arises  at  the  level  of  the  third  costal  cartilage  behind  the  sternum. 
It  reaches  halfway  up  the  manubrium,  and  is  nearest  the  surface  at  the 
second  right  costal  cartilage. 


152 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


The  Valves. — The  aortic  valve  lies  behind  the  third  left  costo-sternal 
junction.  It  is  one-fourth  overlapped  by  the  pulmonary  valve.  The 
pulmonary  valve  lies  a  little  higher  and  more  to  the  left.  The  mitral  valve 
lies  behind  the  third  intercostal  space  about  1  inch  to  the  left  of  the  ster- 
num.    The  tricuspid  valve  lies  below  and  slightly  to  the   left  of  a  line 


Fig  125. — Radiogram  showing  the  relative  position  of  the  cardiac  valves  in  relation  to 
each  other  and  to  the  anterior  bony  thorax.  The  pulmonary,  in  part  overlies  the  aortic, 
valve.     It  is  the  most  superficially  placed  of  all  the  heart  valves.      The  mitral  valve  is  the 

fnr  +  li  oc?+-    -fr-*-M-»-i     4-\i  a     on  +  orini'    c»Vi  not     tttoH  TVi  a    lovnrn    0170    nf      +Viq    tri^iitnirl     ni'ifi  no    1C     Tirol  1     ch  nwn 


drawn  from  the  inner  end  of  the  third  left,  to  the  sixth  right  costal  carti- 
lages. The  aortic,  mitral  and  tricuspid  valves  are  anatomically  practi- 
cally contiguous  structures.  The  mitral  is  the  furthest  from,  the  pul- 
monic the  nearest  to,  the  anterior  chest  wall  (Figs.  123,  128). 

Posteriorly. — The  base  of  the  heart  lies  at  the  level  of  the  fifth  dorsal 

1Norris  and  Fetterolf:  "The  Topography  of  the  Cardiac  Valves  as  Revealed 
by  the  X-rays."     Am.  Jour.  Med.  Sc,  cxlv,  1913,  225. 


THE    CIRCULATORY    SYSTEM 


153 


. 


;\ 


P*\ « :v 


\ 


Left  innom- 
inate vein 


r  Right  auricle 


Papillary 

muscle * 


Right  ventrii 


Right  pulmo- 
nary artery 
Descending 
aorta 
Left  bronchus 


Aortic  leaflets 


Left  lung 


Fig.  126. 


154 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


•:•-•/  si 


Aorta 


Right  pul.  artery 


Left  super,  pul.  vein 

L.  auricular  appendix  ; 

L.  infer,  pul.  vein  ■ 

Left  auricle  ' 


Mitral    valve    ante- 
rior leaflet 


'/' 


Aortic  leaflets 


Left  ventricle 
Right  ventricle 


Fig.  127. 

Figs.  126  and  127. — These  sections  show  the  deeply  placed  position  of  the  left  auricle 
which  may  be  topographically  described  as  the  "posterior  auricle."  They  also  depict  the 
relatively  large  amount  of  mediastinal  space  which  is  occupied  in  an  antero-posterior  di- 
rection by  the  heart.  The  rear  view  of  the  heart  is  shown  in  Figs.  91  and  92,  the  anterior 
aspect  in  Figs.  86  and  163. 


THE    CIRCULATORY    SYSTEM  155 

vertebra.  The  apex  of  the  heart  lies  at  the  level  of  the  eighth  dorsal  ver- 
tebra. The  aorta  reaches  the  spine  at  the  level  of  the  fourth  dorsal 
vertebra.  The  pulmonary  artery  bifurcates  at  the  level  of  the  fourth 
dorsal  vertebra.  Practically  the  whole  anterior  surface  of  the  heart  is 
right  heart  (see  Fig.  163).  The  left  auricle  lies  posteriorly.  Of  the  left 
ventricle  only  the  tip  is  seen  from  in  front. 


-—.it 


Fig.  12S. — Diagram  illustrating  the  relative  position  of  the  heart  valves  as  seen  from 
above:  1.  pulmonary;  2,  aortic;  3,  mitral;  4,  tricuspid.  The  pulmonary  is  the  most  super- 
ficial, and  the  mitral  the  most  deeply  placed  of  the  cardiac  valves  (comp.  Fig.  123). 

PALPATION  OF  THE  PULSE 

The  pulse  is  generally  examined  by  palpation  of  the  radial  artery. 
When  the  patient's  hands  are  not  accessible,  as  during  sleep,  the  temporal 
artery  is  often  selected.  Under  certain  circumstances  it  may -be  neces- 
sary to  feel  the  pulse  elsewhere  as,  for  instance,  in  the  tibial  arteries  or 
in  the  dorsalis  pedis.  The  pulse  should  be  palpated  with  the  tips  of  the 
fingers,  not  with  the  palmar  surface.  The  thumb  must  not  be  used 
because  a  subjective  pulse  can  often  be  felt.  When  examining  the  pulse 
two  conditions  are  to  be  determined:  (1)  the  character  of  the' arterial  wall 
(arterio-sclerosis,  etc.) ;  and  (2)  the  character  of  the  pulse. 

1.  Arterial  thickening  is  determined  (a)  by  rolling  the  emptied  artery, 
in  which  the  blood  flow  has  been  temporarily  occluded  by  pressure  above 
and  below  the  point  of  palpation,  under  the  ball  of  the  finger;  (6)  by  allow- 
ing the  end  of  the  finger  nail  to  slip  across  the  arterial  wall.  Normal 
arteries  are  barely  palpable. 

An  important  source  of  error,  however,  lies  in  the  state  of  vascular 
tonus.  When  blood-pressure  is  high  the  artery  may  readily  be  rolled 
under  the  finger,  and  the  tactile  sensation  received  may  be  similar  to  that 
produced  by  actual  arterial  sclerosis.  Increased  tonus  may  sometimes 
be  temporarily  abated  by  local  massage  of  the  artery.  On  the  other 
hand,  a  definitely  thickened  artery  may  escape  detection  when  tonus  is 
diminished. 

If  arterio-sclerosis  is  suspected,  examination  must  not  be  limited  to 
the  radial  arteries  but  should  include  the  brachials,  femorals,  temporal 
and  retinal  arteries  as  well. 

2.  The  character  of  the  pulse  is  judged  by  noting  the  rate,  rhythm, 
volume,  tension  and  equality.  Both  radial  arteries  should  be  habitually 
palpated  synchronously  in  order  to  determine  bilateral  equality. 


156  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

The  Pulse  Rate. — The  normal  rate  in  adults  is  for  men  72,  for  women 
80.  With  advancing  years  the  rate  often  becomes  slower.  Certain 
individuals  in  perfect  health  may  have  by  nature  a  rapid  (90)  or  a  slow 
(60-70)  pulse.  The  latter  rate  is  not  infrequent  in  advanced  years.  In 
the  new-born  the  rate  averages  about  140,  and  at  fourteen  years  about  90. 
The  pulse  rate  is  increased  by  excitement,  anger,  fear,  exercise,  digestion, 
deep  inspiration,  low  blood-pressure,  fever,  etc.  The  pulse  increases 
about  ten  beats  for  every  degree  Fahrenheit  above  the  normal  body 
temperature.  It  is  more  rapid  in  short,  high-strung  individuals  than  in 
people  with  a  large  frame  and  a  phlegmatic  disposition.  The  peripheral 
pulse  rate  does  not  always  indicate  the  cardiac  rate.  Xotable  discrep- 
ancies may  occur  in  auricular  fibrillation,  extrasystolic  arrhythmia  and 
pulsus  alternans.  The  complete  bodily  circuit  of  blood  flow  requires 
normally  about  23  seconds  and  is  accomplished  by  about  27  systoles. 
The  pulse  wave  travels  9  to  10  m.  per  second,  it  therefore  reaches  the 
dorsalis  pedis  artery  3i5  second  later  than  the  aorta — about  the  middle 
of  ventricular  systole.  The  time  required  to  reach  the  radial  artery  is 
approximately  0.17,  and  the  interval  between  the  carotid  and  the  radial 
pulses,  is  0.08  second. 

Tachycardia. — This  term  is  generally  applied  to  a  pulse  rate  above 
130  per  minute.  It  may  occur  in  exophthalmic  goitre,  in  cardiac  disease, 
in  vasomotor  collapse,  etc.,  but  is  most  characteristically  seen  in  "paroxys- 
mal tachycardia,"  a  condition  due  either  to  extrasystoles  or  to  a  fibrillat- 
ing  auricle. 

Bradycardia. — This  term  is  generally  applied  to  a  pulse  rate  of,  or  of 
less  than,  60  per  minute.  It  may  occur  in  convalescence,  after  vomiting, 
in  basilar  meningitis  or  increased  intracranial  pressure  (vagus  irritability 
or  stimulation)  and  also  in  jaundice  (toxic  effect).  It  occurs  character- 
istically in  heart  block,  in  which  condition  it  may  fall  to  twelve  beats 
per  minute. 

The  Pulse  Rhythm. — The  pulse  may  be  irregular  either  in  regard  to 
(1)  time  or  (2)  force.  Xot  infrequently  both  factors  are  combined,  as  in 
auricular  fibrillation  (see  Cardiac  Arrhythmia). 

The  Pulse  Volume. — The  volume  of  the  pulse  is  gauged  by  estimating 
the  degree  of  pulsatile  oscillation — the  amount  of  systolic  filling  and  the 
completeness  of  diastolic  collapse.  It  depends  upon  and  is  in  part  a 
measure  of  the  systolic  output.  The  pulse  pressure — the  difference  be- 
tween the  systolic  and  the  diastolic  pressures — may  be  taken  as  a  rough 
index  of  pulse  volume.  As  a  general  rule  the  more  rapid  the  rate,  the 
smaller  the  volume  of  the  pulse. 

The  Pulse  Tension. — This  is  estimated  by  gauging  the  amount  of 
pressure  which  must  be  exerted  upon  the  artery  before  the  flow  of  blood 
is  stopped.  In  other  words  it  depends  upon  the  blood-pressure  which  is 
due  chiefly  to  vascular  tonus,  cardiac  force  and  valvular  sufficiency.  The 
pulse  is  sometimes  described  as  hard  or  soft,  depending  upon  whether 
arterial  tension  is  high  or  low.  These  terms  are  obsolete,  the  degree  of 
tension  should  be  measured  with  a  sphygmomanometer  and  the  height 
of  the  systolic  and  the  diastolic  pressures  recorded  in  millimeters  of 
mercury  (see  Blood-pressure  Instruments,  p.  161).  The  celerity  of  the 
pulse  wave  depends  upon  the  suddenness  of  its  collapse.  A  "quick" 
pulse  is  not  a  rapid  pulse,  but  one  which  disappears  quicklj'.  It  occurs 
characteristicallv  in  aortic  insufficiencv  and  is  known  as  the  water-ham- 


THE    CIRCULATORY    SYSTEM 


157 


mer  or  Corrigan  pulse,  but  it  also  occurs  in  a  minor  degree  in  severe  anemia 
and  in  vasomotor  paresis. 

The  opposite  condition — pulsus  tardus — appears  and  disappears 
slowly.  The  systolic  ascent  of  the  sphygmogram  is  gradual,  the  plateau 
long  and  the  descent  prolonged.  This  type  of  pulse  is  observed  es- 
pecially in  aortic,  and  in  a  minor  degree  mitral,  obstruction.  It  is  a 
valuable  diagnostic  sign  of  the  former. 

The  Equality  of  the  Pulse. — By  this  we  mean  equality  in  (1)  volume, 
(2)  time  and  (3)  force,  in  symmetrical  arteries  of  the  body.  Inequality 
of  the  radial  arteries  may  result  from:  (1)  surgical  injuries  of  the  upper 
extremities,  (2)  axillary  growths,  (3)  aneurism  of  the  aorta,  innominate, 
subclavian,  brachial  or  radial  arteries,  (4)  emboli  or  thrombi  or  syphilitic- 
disease  in  these  arteries,  (5)  massive  pleural  effusions,  (6)  local  inflam- 
matory conditions,  (7)  extreme  auricular  dilatation.  Slight  degrees  of 
inequality  occur  very  commonly.  This  sign  is  of  little  importance  unless 
it  is  well  marked.1 

NORMAL  AND  ABNORMAL  TYPES  OF  THE  ARTERIAL  PULSE 

The  normal  arterial  pulse  which  is  felt  as  a  single  "beat"  consists 
when  analyzed  of  the  following  waves: 


*i  Settle' 2K*-stole. 


Fig.  130. — The  normal  radial  curves: 
a-b,  the  tidal  wave;  b-e,  the  aortic  notch;  g, 
the  dicrotic  wave;  h,  the  post-dicrotic  wave. 


Fig.  129. — The  cardiogram  (tracing  from 
the  precordium) :  a,  auricular  wave;  c.d.~ 
e.f.,  ventricular  systole) ;  d,  marks  the  open- 
ing and  /,  the  closure  of  the  semilunar  valves, 
(beginning  of  diastole) ;  k,  sudden  ventricular 
filling. 

The  arterial  pulse,  by  which  term  we  designate  the  expansion  and 
contraction  of  an  artery  which  occurs  during  the  systole  and  diastole  of 
the  heart,  has  long  been  used  as  a  diagnostic  criterion.  When  the  sphyg- 
mograph  was  first  introduced  in  medicine  it  was  hoped  that  a  detailed 
study  of  the  length,  height  and  time  relations  of  the  various  phases  of 
the  pulse  tracing  would  lead  us  far  toward  perfection  in  diagnosis.  As  a 
result  of  such  studies  many  different  types  of  the  arterial  pulse  were 
classified,  named  and  studied,  though  with  but  little  practical  result. 
Such  studies  do,  of  course,  enable  us  to  visualize  our  palpatory  sensations, 
but  the  value  of  the  sphygmogram  to-day  lies  almost  wholly  in  the  time 
relationship  between  the  arterial  and  the  venous  pulse  waves.  There 
are,  however,  certain  types  of  the  arterial  pulse  which  arc  more  or  less 
characteristic  of  certain  conditions  which  find  a  place  in  clinical  nomen- 

1  In  a  study  of  500  cases  (well  and  ill)  the  two  radial  pulses  were  alike  in  only  56 
per  cent.  There  was  marked  difference  in  2.5  per  cent.  The  left  pulse  was  stronger  in 
14  per  cent,  of  455  right-handed  people,  and  in  43  per  cent,  of  the  21  ambidextrous. 
In  advanced  life  inequality  is  generally  due  to  arteriosclerosis  (Koennicke:  Therap. 
d.  Gegeniv.,  September,  19ll). 


158  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

clature  and  are  recognizable  by  the  sense  of  touch.     Among  these  the 
following  may  be  mentioned : 

The  Dicrotic  Pulse, — A  dicrotic  pulse  is  one  of  low  tension  in  which 
the  normal  secondary  wave  becomes  exaggerated,  so  that  it  may  be  both 
felt  and  instrumentally  demonstrated  to  consist  of  a  more  or  less  separate 
wave.  It  appears,  therefore,  a  repetition  or  echo  of  the  primary  wave. 
If  the  pulse  rate  is  rapid,  the  line  of  descent  of  the  dicrotic  wave  is 
interrupted  by  the  next  primary  wave,  which  condition  is  known  as  anac- 
rotism.  In  the  majority  of  the  febrile  cases  at  least,  it  is  brought  about 
by  relaxation  of  the  arteries  and  constriction  of  the  arterioles,  which 
condition  causes  an  actual  backward  flow  of  blood  in  the  primary  pulse 
wave,  a  phenomenon  which  is  repeated  in  the  case  of  the  dicrotic  wave. 
Other  causes  such  as  a  brief  systolic  output  from  the  heart,  or  dilatation 
of  certain  vascular  areas,  especially  the  splanchnics,  have  been  suggested 
(Hewlett). 

The  Pulsus  Bisferiens. — This  term  should  be  applied  only  to  those 
cases  in  which  the  apices  of  the  two  waves  are  separated  by  a  time  interval 
of  not  less  than  }{q  second,  thus  eliminating  cases  of  mere  clicrotism. 
It  is  usually  associated  with  reduplication  of  the  first  sound,  and  an 
analogous  cardiogram,  being  therefore  central  in  origin.  It  is  uncertain 
whether  the  second  wave  arises  in  the  ventricle  or  in  the  aorta.  It  is 
generally  met  with  in  cases  of  left  ventricular  hypertrophy  in  association 
with  disease  of  the  aortic  valves  of  the  large  arteries.1 

The  Pulsus  Bigeminus. — By  this  term  we  understand  a  type  of  regular 
irregularity  in  which  the  pulse  waves  instead  of  being  equally  spaced 
occur  in  groups  of  two,  to  be  followed  by  a  more  or  less  prolonged  pause 
(see  Extrasystoles) . 

"Ventricular  bigeminy  which  occurs  in  clinical  instances  of  auricular 
fibrillation  either  spontaneously  or  in  the  wake  of  digitalis  administra- 
tion, is  due  to  a  disturbance  of  the  irregular  series  of  responses  to  the 
auricle  by  ectopic  beats  arising  in  the  ventricular  musculature"  (Lewis). 
It  includes  practically  all  instances  of  accurate  coupling.  The  two  beats 
should  bear  a  constant  time  relationship  to  each  other  (Wenckebach). 
If  the  pulse  waves  occur  in  groups  of  three  or  four,  we  describe  it  as  a 
pulsus  tri-  or  quadrigeminus,  respectively. 

The  Water-hammer  Pulse. — The  Corrigan  or  water-hammer  pulse 
occurs  chiefly  and  most  characteristically  in  aortic  insufficiency.  It  is 
quick,  collapsing  and  large  in  volume.  The  diastolic  pressure  is  always 
low  (60  to  40  mm.  Hg.),  and  the  systolic  pressure  generally  high  (180  to 
140  mm.  Hg.).  Diastole  is  shortened  and  the  height  of  the  secondary 
wave  is  in  direct  proportion  to  the  amount  of  arterio-sclerosis  present, 
and  not  to  that  of  the  blood-pressure  (Lewis). 

The  Pulsus  Paradoxus. — This  term  is  applied  to  the  disappearance  or 
enfeeblement  of  the  pulse  during  inspiration. 

It  may  occur  normally: 

(1)  During  deep  inspiration  with  glottis  closed — negative  intrathoracic  pressure 
(Mueller's  experiment).  (2)'  During  forced  expiration  with  closed  glottis — high 
intrathoracic  pressure  (Valsalva's  experiment).  (3)  If  the  breath  is  held  after  a 
forced  inspiration — pressure  on  the  subclavian  artery — glottis  open.  (The  muscles 
of  shoulder  girdle  compress  the  subclavian  artery  between  the  clavicle  and  the  first 
rib.) 

1  Lewis,  T.:  Brit.  Med.  Jour.,  April  20,  1907. 


THE    CIRCULATORY    SYSTEM 


159 


Normal  sphygmogram. 


The  dicrotic  pulse   (8th  clay  of  pneumonia). 


Pulsus  bisferiens. 


The  bigeminal  pulse  (digitalis  effect  in  auricular  fibrillation). 


The  water-hammer  pulse  (aortic  insufficiency). 


Slow  high  tension  pulse  (arteriosclerosis). 


Pulsus  irregularis  perpetuus  (auricular  fibrillation).      Irregular  both  as  to  time  and  volume. 

Fig.  131. 


160  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

It  may  occur  pathologically: 

(1)  At  the  extremes  of  life  during  inspiration.  (2)  During  inspiratory  dyspnea — 
croup — slow  inspiration,  high  negative  intrathoracic  pressure.  (3)  In  cases  of  ad- 
hesive (mediastino)  pericarditis.  Respiratory  traction  resulting  from  mediastinal 
adhesions,  is  brought  to  bear  on  some  of  the  large  vessels.  (It  may  be  a  unilateral 
phenomenon.)  If  enfeeblement  or  disappearance  occurs  during  expiration  it  is 
called  Riegel's  pulse.  The  paradoxical  pulse  has  little  if  any  pathologic  significance. 
The  pathological  paradoxic  pulse  is  generally  assumed  to  be  due  to  constriction  of 
some  of  the  large  vessels  by  mediastinal  adhesions.  The  paradoxic  venous  pulse- 
filling  of  the  veins  during  inspiration — has  a  similar  genesis. 


CHAPTER  XIV 

INSTRUMENTAL  METHODS,  BLOOD-PRESSURE  ESTIMATION 

Pulse  tension  or  blood-pressure  is  best  estimated  by  means  of  a 
mercurial  sphygmomanometer  equipped  with  a  cuff,  not  less  than  12  cm. 
in  width.     For  children  smaller  sizes  may  be  employed. 

TECHNIC 

The  Systolic  Pressure. — The  cuff  is  applied  snugly  to  the  upper  arm 
and  secured  by  means  of  straps  or  a  bandage.  The  cuff  is  then  connected 
with  the  manometer  and  quickly  inflated  to  a  point  well  above  the  sys- 


Fig.   132. — The  Uskoff  sphygmotonograph. 

tolic  pressure,  after  which  the  stop-cock  is  turned,  so  as  to  exclude  the 
pump  from  communication  with  the  cuff.  A  stethoscope  is  now  placed 
over  the  brachial  artery  below  but  not  in  contact  with  the  cuff,  and  auscul- 
tation is  practised  while  the  pressure  is  gradually  allowed  to  fall.  The 
first  clear  thumping  or  pounding  noise  indicates  the  fact  that  pressure  in 
the  artery  is  now  sufficiently  high  to  force  the  blood  under  the  constricting 
cuff,  and  to  distend  the  artery  below.  The  height  of  the  mercurial 
11  161 


162  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

column  at  which  this  acoustic  phenomenon  occurs  indicates  the  systolic 
-pressure  in  the  brachial  artery. 

The  Diastolic  Pressure. — The  examiner  should  continue  to  listen 
while  the  mercury  falls,  and  in  doing  so  will  notice  after  a  time,  that  the 
thumping  sound  is  followed  by  a  "hiss"  or  murmur  which  in  turn  dis- 
appears and  is  replaced  by  a  clear-cut  sound  similar  to  that  first  heard. 
As  the  mercury  falls  still  lower  this  clear-cut  sound  suddenly  becomes 
muffled  and  distant.  This,  the  beginning  of  the  fourth  auscultatory  phase, 
indicates  the  diastolic  pressure. 

Occasionally  it  happens  that  the  fourth  phase  cannot  be  accurately 
identified.  In  such  cases  the  fifth  phase  (the  disappearance  of  all  sound) 
is  chosen  as  the  diastolic  criterion.  The  difference  between  these  two 
phases  rarely  exceeds  a  few  millimeters  of  mercury,  but  at  times  they 
may  be  separated  by  15  mm.  or  more.  The  fifth  phase  is  sometimes 
persistent  down  to  0  mm.  Hg.  in  aortic  insufficiency.  In  these  cases  the 
diastolic  pressure  must  be  estimated  by  the  fourth  phase  or  not  by 
auscultation  at  all. 

For  purposes  of  comparison,  blood-pressure  readings  should  be  made 
(1)  in  the  same  posture;  (2)  on  the  same  arm;  (3)  in  about  the  same 
relation  to  meals.  It  should  be  remembered  that  pain,  fear,  anxiety, 
excitement,  exercise,  etc.,  may  cause  marked  increase  in  pressure  although 
in  such  instances  it  is  the  systolic  pressure  which  is  chiefly  affected.  The 
readings  should  be  made  as  quickly  as  is  consistent  with  accuracy.  After 
estimating  the  pressure  the  air  should  be  allowed  to  escape  from  the  cuff 
and  after  the  lapse  of  a  few  minutes  a  control  observation  should  be  made. 
This  will  often  be  found  to  be  lower  than  the  first  reading,  especially 
in  patients  unaccustomed  to  the  procedure,  the  initial  high  reading  being 
due  to  psychic  influences.  If  the  cuff  remains  inflated  for  too  long  a 
time,  the  resultant  venous  stasis  will  per  se  increase  the  pressure. 

NORMAL  BLOOD-PRESSURE 

In  healthy  adults  the  normal  systolic  pressure  is  about  130,  the 
diastolic  pressure  about  80  mm.  Hg.  During  the  first  month  of  life  the 
systolic  pressure  ranges  between  60  and  90  mm.  Hg.  and  gradually  in- 
creases. This  increase  bears  a  more  constant  relation  to  height  and 
weight  than  to  age  or  sex.  The  diastolic  pressure  in  infants  is  very 
difficult  to  estimate  owing  to  the  small  size  and  relatively  deep  situa- 
tion of  the  artery. 

As  age  increases  pressure  gradually  tends  to  rise,  generally  at  the 
ratio  of  about  1  mm.  Hg.  for  every  two  years  of  life,  assuming  that  a 
youth  of  twenty  years  has  a  pressure  of  120  mm.  Hg.  Pressure  readings 
above  160  mm.  (systolic)  or  ioo  mm.  (diastolic)  if  constantly  present 
must  be  considered  pathologic  at  any  age. 

THE  SIGNIFICANCE   OF  BLOOD-PRESSURE  ABNORMALITIES 

Increased  blood-pressure  is  clinically  more  common  and  diagnostically 
far  more  significant  than  decreased  blood-pressure. 

Hypotension. — Occurs  chiefly  in  early  life  (constitutional  or  essential 
hypotension)  and  is  often  associated  with  visceroptosis  and  sometimes 
with  tuberculous  disease.  It  is  also  met  with  after  exhausting  fevers, 
in  cachexia,  as  a  terminal  phase  of  hypertension,  and  in  shock. 


INSTRUMENTAL   METHODS,    BLOOD-PRESSURE    ESTIMATION 


163 


Fig.  133. — The  Jacquet  cardiosphygmograph.      The  jugular  vein  on  the  right,  and  the  caro- 
tid artery  on  the  left  as  well  as  the  radial  pulse  are  being  simultaneously  recorded. 


Fig.  134. — The  Jacquet  cardiosphygmograph.  A  detailed  view  of  the  instrument, 
showing  special  apparatus  for  steadying  the  hand  and  throwing  the  radial  artery  into  more 
close  contact  with  the  receiver. 


164  THE    EXAMINATION    OF    CIRCULATOEY    SYSTEM 

Hypertension. — Occurs  chiefly  after  middle  life  and  suggests  the  clini- 
cal symptom  complex  known  as  Bright's  disease — arteriolar  disease  with 
cardiac  hypertrophy  and  more  or  less  destruction  of  renal  tissue,  ter- 
minating in  cardio-vascular  failure,  uremia,  apoplexy  or  angina  pectoris. 
Hypertension  may  also  occur  in  plumbism,  polycythemia,  etc.,  or  it 
may  be  temporarily  present  as  the  result  of  anger,  fright,  excitement  or 
physical  exercise.  It  may  occur  locally  as  a  result  of  vascular  spasm 
(vascular  crises)  and  cause  intermittent  claudication,  blindness,  aphasia, 
angina  pectoris,  etc. 

VENOUS    BLOOD-PRESSURE 

The  clinical  estimation  of  venous  blood-pressure  is  attended  with  much 
more  difficulty  and  much  less  accuracy  than  in  the  case  of  arterial  ten- 
sion. A  rough  clinical  test  may  be  made  by  noting  the  level  at  which 
the  veins  of  the  hand  collapse  while  the  arm  is  being  gradually  raised 
from  the  level  of  the  hip  to  above  that  of  the  shoulder.  Collapse  normally 
should  occur  at  xipho-sternal  articulation  (Gaertner's  test).  Venous 
pressure  is  estimated  in  centimeters  of  H20.  The  normal  pressure  at 
the  level  of  the  auricles  (Louis'  angle)  ranges  between  5  and  10  cm.  H20. 
It  is  increased  by  exercise,  weakness  of  the  right  heart,  etc.,  and  may 
reach  as  high  a  figure  as  30+  cm.1  An  increase  in  venous  pressure 
generally  occurs  with  a  fall  of  arterial  pressure  when  cardiac  compensation 
fails. 

THE  VENOUS  PULSE 

Relatively  little  knowledge  can  be  derived  from  a  sphygmographic 
tracing  of  the  arterial  pulse  alone,  but  combined,  simultaneous  records 
taken  from  the  jugular  vein  and  from  the  radial  or  brachial  artery  are 
often  of  extreme  importance  and  are,  indeed,  the  chief  method  by  which 
the  different  forms  of  cardiac  arrhythmia  are  clinically  studied.  The 
phlebogram  from  the  jugular  vein  depicts  the  activity  of  the  right  auricle, 


Fig.    185. — Normal  phlebogram. 

the  sphygmogram  of  the  brachial  artery  that  of  the  left  ventricle.  The 
cardiogram — the  tracing  taken  from  the  apex  impulse — is  often  un- 
satisfactory and  clinically  of  minor  importance. 

The  normal  venous  pulse  consists  of  three,  sometimes  of  four  curves. 

The  "a"  wave  is  a  stasis  wave  due  to  the  contraction  of  the  right 
auricle.  It  is  presystolic  in  time.  The  "c"  wave  is  a  true  venous  wave 
due  to  contraction  of  the  right  ventricle,  but  in  clinical  tracings  made 
over  the  jugular  vein  this  wave  is  in  part  due  to  the  impulse  transmitted 
from  the  neighboring  carotid  artery.  The  interval  which  elapses  be- 
tween the  beginning  of  the  "a"  and  the  "c"  waves  is  known  as  the  con- 
duction time.     It  represents  the  length  of  time  required  for  the  stimulus 

1  For  more  detailed  information  see  Norris,  G.  W. :  "Blood-pressure,  Its  Clinical 
Application,"  Philadelphia,  1916. 


INSTRUMENTAL    METHODS,    BLOOD-PRESSURE    ESTIMATION  165 

which  causes  the  heart  to  contract  to  pass  from  the  auricles  through  the 
auriculo-ventricular  bundle  to  the  ventricles  and  to  produce  contrac- 
tions in  these  chambers.  The  time  normally  required  is  0.2  second 
with  a  pulse  rate  of  80  per  minute.  An  increase  of  the  "a-c"  time 
often  indicates  a  lesion  in  the  bundle  of  His. 

The  "v"  wave  is  a  stasis  wave  which  occurs  while  the  ventricle  is 
filling  with  blood,  and  which  disappears  suddenly  when  the  auriculo- 
ventricular  valves  open.  The  "v"  wave  occurs  early,  is  large  and  pro- 
longed when  the  right  ventricle  is  overloaded.  In  cases  of  tricuspid 
insufficiency  the  "c"  wave  disappears  and  is  supplanted  by  a  large  "v" 
wave.  The  venous  pulse  under  these  circumstances  is  spoken  of  as  a 
"positive  venous  pulse." 

The  "h"  wave  is  not  normally  present.  It  is  due  to  a  flapping  to- 
gether (upward)  of  the  tricuspid  and  mitral  leaflets,  and  is  protodiastolic 
in  time.  It  is  synchronous  with  the  third  heart  sound  and  may  occur 
(1)  in  slowly  beating  hearts  (because  of  relatively  early  diastolic  ven- 
tricular distention);  (2)  in  aortic  insufficiency  (because  of  high  intra- 
ventricular pressure) ;  (3)  in  the  early  stages  of  mitral  stenosis  (rapid 
ventricular  rilling  clue  to  a  distended  auricle). 

SPHYGMOGRAPHS 

Numerous  instruments  have  been  devised  for  the  recording  of  arterial 
and  venous  pulse  waves.  The  authors  personally  prefer  the  Uskoff 
spkygmotonograph,  which  may  be  obtained  either  with  or  without  a 
manometer  for  estimating  blood-pressure.  The  driving  mechanism 
which  propels  the  smoked  paper  is  equipped  with  two  speeds  and  very 
excellent  records  from  the  brachial  artery  and  the  jugular  vein  can  be 
made  in  a  very  few  minutes. 

The  Jacquet  cardio-sphygmograph  has  the  advantage  of  permitting 
one  to  make  three  simultaneous  records,  but  as  already  stated  the  car- 
diogram is  of  little  value  in  the  average  case.  The  respiratory  movements 
can,  however,  be  traced  instead  of  the  cardiac  impulse.  Like  all  instru- 
ments which  are  attached  to  the  wrist,  the  adjustment  is  more  trouble- 
some and.  more  time  is  required  to  make  a  tracing. 

The  Mackenzie  polygraph  is  much  used,  but  in  our  experience  the 
jugular  tracing  is  not  as  satisfactory  as  with  the  above-mentioned  in- 
struments, and  a  good  deal  of  time  is  sometimes  required  for  adjustment. 
The  tracings  are  made  with  ink  pens  upon  white  paper  which  runs  off  a 
spool,  so  that  very  long  tracings  can  be  made.  This  is  a  feature  of  un- 
doubted utility  in  some  cases. 

General  Technique. — For  the  purpose  of  making  jugular  tracings  the 
patient  must  be  in  the  recumbent  position,  with  the  head  as  low  as 
possible.  A  small  pillow  under  the  head,  however,  is  sometimes  neces- 
sary, in  order  to  relax  the  sternomastoid  muscle  at  the  origin  of  which 
the  receiver  is  placed.  When  respiratory  excursions  are  deep,  it  is  often 
necessary  for  the  patient  to  hold  his  breath  while  the  phlebogram  is  being 
made,  since  the  oscillation  of  the  supraclavicular  structures  may  confuse 
the  venous  waves.  The  Uskoff  cuff  requires  no  adjustment  other  than 
inflation  to  about  the  level  of  the  diastolic  pressure.  With  the  Jacquet 
instrument,  however,  the  receiver  must  be  placed  exactly  over  the  radial 
artery.     If  the  course  of  the  artery  is  outlined  upon  the  skin  by  means  of 


166 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


a  blue  pencil,  this  procedure  is  much  facilitated.     The  patient  must  be 
cautioned  not  to  move  the  hand  once  the  instrument  has  been  adjusted. 

The  cardiogram  should  be  taken  over  the  outermost  portion  of  the 
apex  impulse.  In  many  cases  no  impulse  may  be  perceptible  unless  the 
patient  rolls  more  or  less  upon  his  left  side.     The  cardiogram  of  the 


Right  int.  jugular  vein. 


Fig.  136. — The  right  internal  jugular  vein  empties  through  the  right  innominate  vein 
into  the  superior  vena  cava.  The  distance  between  the  jugular  bulb  over  which  phlebo- 
grams  are  taken  is  not  far  from  the  right  auricle  and  since  no  venous  valves  are  interposed, 
auricular  pressure  changes  promptly  produce  relatively  similar  changes  in  the  jugular  vein. 


right  ventricle  may  often  be  obtained  in  or  near  the  epigastrium.  In 
contradistinction  to  that  of  the  left  ventricle  it  consists  of  a  systolic 
retraction,  not  an  elevation. 

The  respirations  may  be  charted   by  placing  a  cup  receiver  in  the 
episternal  notch  or  by  placing  the  cardiograph  attachment  in  the  epigas- 


INSTRUMENTAL    METHODS,    BLOOD-PRESSURE    ESTIMATION  167 

trium  and  maintaining  it  in  position  by  means  of  an  elastic  strap.  The 
registration  of  the  respiratory  curve  is  chiefly  important  in  relation  to 
sinus  arrhythmia.  In  most  of  the  instruments  in  clinical  use  the  time  is 
recorded  in  fifths  of  a  second. 

It  is  necessary  that  either  (1)  the  recording  needles  be  directly  in  line 
where  the  tracing  is  made,  or  (2)  that  any  discrepancy  which  may  exist 
between  their  position  be  shown  upon  the  tracing  so  that  allowance  may 
be  made  for  it  in  identifying  the  venous  waves.  This  is  shown  in  Fig. 
137  in  which  the  driving  mechanism  has  been  stopped  near  the  middle 
of  the  tracing  and  the  relative  position  of  the  recording  needles  is  shown 
by  the  vertical  strokes  of  the  lever. 

THE  INTERPRETATION  OF  PULSE  TRACINGS 

First. — The  first  point  requiring  attention  is  the  identification  of  the 
"c"  wave  in  the  jugular  tracing.  This  is  accomplished  by  selecting  the 
wave  which  very  slightly  precedes  the  .systolic  wave  in  the  brachial 
tracing.  In  doubtful  cases  the  receiver  may  be  moved  up  higher  along 
the  edge  of  the  sternomastoid  muscle  where  a  pure  carotid  tracing  can  be 
obtained. 

Second. — The  "a"  wave  is  identified  by  the  fact  that  it  immediately 
precedes  the  "c"  wave.  It  appears  from  0.15  to  0.2  second  before  the 
latter  and  almost  synchronously  with  the  "a"  wave  of  the  cardiogram 
since  there  are  no  venous  valves  interposed  between  the  right  auricle 
and  the  jugular  bulb  (see  Fig.  137). 

Third. — The  "'v"  wave  follows  the  ac"  wave  after  a  variable  interval. 
It  is  often  separated  from  the  former  by  a  sharp  negative  depression 
"x"  which  is  chiefly  due  to  negative  auricular  pressure  due  to  displace- 
ment of  the  auriculo-ventricular  tissues  during  ventricular  systole. 

The  "v"  wave  is  sometimes  split,  the  first  portion  "y"  being  due  to 
ventricular  systole  and  occurring  during  the  latter  part  of  the  systolic 
plateau  in  the  cardiogram.  The  second  portion  "v2"  occurs  at  the  end 
of  this  time  and  is  due  to  the  downward  rebound  of  the  auriculo- 
ventricular  tissues  to  their  normal  position. 

The  second  negative  depression  "y"  is  due  to  the  opening  of  the 
auriculo-ventricular  valves. 


CHAPTER  XV 

CARDIAC  ARRHYTHMIA 

Recent  additions  to  our  knowledge  of  cardiac  anatomy  and  physi- 
ology have  thrown  much  valuable  light  upon  our  conception  of  heart 
disease,  and  have  placed  cardiac  diagnosis  and  therapy  upon  a  much 
more  accurate  scientific  basis.  As  a  result  of  these  advances  the  study 
of  cardiac  irregularities  has  been  greatly  simplified,  and  the  classifica- 
tion of  these  conditions  has  changed  from  the  hopeless  jumble  which 
existed  a  few  years  ago,  to  a  small  and  relatively  simple  grouping. 

NORMAL  RHYTHM 

The  stimulus  which  causes  the  heart  to  contract  arises  in  the  sino- 
auricular  node,  a  small  collection  of  specialized  right  auricular  tissue 
which  lies  "in  the  sulcus  terminalis  just  below  the  fork  formed  between 
the  superior  surface  of  the  auricular  appendix  and  the  superior  vena 
cava." 


Fig.  137. — Normal  phlebogram.  Blood-pressure  S.  130,  D.  78  mm.  Hg.  Note  the  regu- 
lar sequence  of  the  "a,"  "c,"  "v"  waves  bearing  a  definite  time  relationship  to  the  brachial 
arterial  waves.     The  conduction  time  ("  a-c  "  interval)  is  normal. 

The  impulse  is  conducted  from  the  auricles  to  the  ventricles  by  means 
of  the  auriculo-ventricular  bundle  (His'  bundle),  a  network  of  specialized 
tissue  which  begins  in  the  right  posterior  margin  of  the  base  of  the 
interauricular  septum  (the  auriculo-ventricular  or  Tawara's  node)  and 
narrowing  to  form  a  bundle  of  fibers,  leads  through  the  interventricular 
septum  to  the  ventricles.  Before  entering  these  structures  it  divides 
into  two  branches  (a  right  and  a  left)  and  again  spreads  out  into  a  net- 
work which  is  distributed  to  the  papillary  muscles  and  to  the  ventricular 
walls,  and  causes  a  contraction  of  these  structures. 

168 


CARDIAC    ARRHYTHMIA  169 

Normal  cardiac  contraction  is  due  to  the  fact  that  this  organ  possesses 
the  functions  of  (1)  stimulus  production,  (2)  excitability,  (3)  conductivity, 
(4)  contractility,  and  perhaps  (5)  tonicity.  Further,  that  these  functions 
are  definitely  coordinated.  The  cardiac  nerves  have  apparently  both  a 
direct  and  an  indirect  modifying  and  controlling  function. 

If  any  portion  of  the  foregoing  mechanism  fails  in  its  proper,  coordi- 
nated function  either  from  the  standpoint  of  time,  place,  or  intensity, 
arrhythmia  will  result.  Thus,  for  instance,  the  stimulus  may  be  generated 
too  rapidly,  or  from  abnormal  regions  (heterogenetic  stimuli),  as  in 
auricular  fibrillation,  so  that  the  ventricles  cannot  keep  pace.  Or  it 
may  be  that  the  auriculo-ventricular  bundle  is  diseased  and  fails  to  con- 
duct impulses  normally  from  the  sinus  node  to  the  ventricles,  and  heart 
block  results.  Again,  the  excitability  of  the  ventricles  may  be  increased 
so  that  they  respond  to  abnormal  stimuli  and  contract  before  the  proper 
time,  producing  ventricular  extrasystoles;  or  the  ventricular  muscle  may 
be  deficient  in  contractile  power  and  contract  with  irregular  force  (pulsus 
alternans). 

The  term  allorhythmia  (altered  rhythm)  is  applied  to  cases  which 
show  a  regular  irregularity  {e.g.,  2  to  1  heart  block)  and  pararhythmia  to 
those  in  which  two  separate  rhythms  are  simultaneously  seen  in  the 
same  or  different  heart  chambers.  Several  different  types  of  irregularity 
may  coincidently  be  present  in  a  given  case.  Thus  extr asystole  not 
infrequently  complicates  the  other  forms.  Among  the  pathologic  types 
of  arrhythmia,  extrasystole  is  the  most  common.  Auricular  fibrillation 
is  next  in  order  of  frequency,  the  third  place  being  filled  by  pulsus  alter- 
nans, and  the  rarest  being  heart  block. 

The  vast  majority  of  cases  of  cardiac  irregularity  will  upon  analysis 
be  found  to  conform  to  one  of  the  following  types.  The  modern  classifi- 
cation of  heart  irregularities,  based  as  it  is  upon  variations  of  definite 
physiologic  functions  of  the  heart  mechanism,  has  greatly  simplified  the 
whole  question. 

SINUS  ARRHYTHMIA 

Under  normal  conditions  a  deep  inspiration  tends  to  accelerate,  a 
deep  expiration,  to  retard  the  pulse.  If  this  condition  becomes  exagger- 
ated so  that,  ordinary  breathing  produces  a  distinct  pulse  irregularity,  we 
speak  of  it  as  sinus  arrhythmia.  The  name  juvenile  arrhythmia  has  also 
been  used  on  account  of  the  frequency  with  which  it  occurs  in  children. 
It  is  essentially  a  vagus  phenomenon,  being  due  to  overactivity  of  the 
tenth  nerve.  Sinus  arrhythmia  may  also  occur  independently  of  the 
respiratory  act.  It  occurs  characteristically  during  convalescence  from 
infections,  can  be  abated  by  full  doses  of  atropin  and  possesses  no  patho- 
logic significance.  Its  recognition  becomes  important  mainly  for  the 
purpose  of  excluding  serious  forms  of  arrhythmia  during  convalescence  in 
diphtheria,  etc.,  or  when  myocardial  disease  is  suspected.  The  heart 
sounds  remain  unaltered  during  sinus  arrhythmia,  only  diastole  being 
affected. 

HEART  BLOCK 

This  form  of  arrhythmia  is  characterized  by  bradycardia  (pulse  rate 
30  to  10  per  minute)  and  by  the  fact  that  venous  pulsations  in  the  jugular 
veins  are  visible  more  frequently  than  ventricular  contractions  over  the 


170 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


precordium.  When  the  bradycardia  is  associated  with  periods  of  asystole, 
syncopal  attacks  or  convulsions,  the  condition  is  known  as  the  Adams- 
Stokes  syndrome.  The  phlebogram  shows  from  two  to  four  "a"  waves 
for  each  "c"  wave.  The  lesion  generally  lies  in  the  auriculo-ventricular 
bundle  and  is  frequently  syphilitic  in  origin.  More  or  less  destruction 
of  the  bundle  " blocks"  the  stimuli  between  the  sinus  node  and  the  ven- 
tricle.    When  the  block  is  complete  the  ventricle  initiates  its  own  rhythm 


y>  /t>«.covt^  s. 


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M 

It 

If.    ■       If 

\-X      11     W      i-p       13,        l.£     0.9 

Fig. 

138- 

—Sinus  arrhythmia, 

showng  pulsie  acceleration  during  inspiration. 

c~       or 


1-0        o<?     o<?     o9     0*9    0  8     Q$    Pf*7   °2 


BRACHIAL. 


Fig.   139. — Auriculo-ventricular  heart  block,  with  the  auricles  beating  twice  as  fast  as  the 
ventricles,  the  rate  of  the  latter  being  30  per  minute. 

(about  30  per  minute).  If  the  block  is  incomplete  every  second,  third, 
or  fourth  sinus  impulse  produces  a  ventricular  contraction  and  the  condi- 
tion is  spoken  of  as  a  2  to  1,  3  to  1,  or  4  to  1,  block.  Incomplete  block 
often  shows  a  prolongation  of  the  "a-c"  interval.  The  conductivity 
time  is  also  frequently  increased  in  rheumatic  valvular  lesions.  The 
abortive  auricular  systoles  can  sometimes  be  heard  over  the  precordium 
as  ill-defined  muffled  heart  sounds.     Heart  block  is  always  serious  and 


CARDIAC    ARRHYTHMIA 


171 


frequently  a  fatal  condition.  Some  seven  cases  of  the  Adams-Stokes  syn- 
drome have,  however,  been  known  to  recover.  Temporary  block  (espe- 
cially in  the  milder  forms  of  prolongation  of  the  "a-c"  interval,  or  an 
occasional  dropped  beat)  may  be  caused  by  full  doses  of  digitalis  and 
similar  remedies.  It  also  may  occur  in  several  of  the  acute  infections, 
especially  rheumatic  fever,  under  which  circumstances  it  is  due  to  acute 
inflammation  of  the  myocardium  of  the  conductive  system. 

EXTRASYSTOLE 

Under  normal  conditions  ventricular  contractions  are  due  to  stimuli 
originating  in  the  sinus  node  and  transmitted  through  the  auricle  and  the 
bundle  of  His  to  the  ventricle.  The  contractions  occur  at  regularly 
spaced  intervals.  Under  abnormal  conditions  additional  effective  stim- 
uli may  arise  at  other  portions  of  the  heart  (auricle,  ventricle,  bundle). 
Such  stimuli  interfere  with  the  regular  rhythm  by  producing  premature 
contractions — extrasystoles.     Such  abnormal  stimuli  are  most  apt  to 


w\v*jr 


JvjtuVaLir 


%*tytf?l~v 


Brachial*        v; 


Fig.   140. — Extrasystoles,  ventricular  in  origin,  followed  by  compensatory  pauses. 


occur  when  the  cardiac  rate  is  slow.  The  muscle  becomes  impatient  in 
waiting  for  its  signal  and  contracts  without  orders.  The  sound  produced 
by  an  extrasystole  is  less  intense  than  the  normal  sound,  and  may  even 
be  inaudible. 

Ventricular  extrasystoles  are  characterized  by  the  fact  that  they  are 
followed  by  compensatory  pauses,  so  that  the  time  occupied  by  the  sys- 
tole and  the  extrasystole  is  equal  to  that  of  two  normal  contractions. 
Also  by  the  fact  that  the  extrasystole  occurs  early  in  diastole  and  pro- 
duces either  a  weak  or  a  missed  beat  at  the  wrist  while  the  succeeding  one 
is  forcible,  so  that  the  patient  is  often  conscious  of  it.  The  compensatory 
pause  is  due  to  the  fact  that  the  next  normal  stimulus  reaches  the  ven- 
tricle so  soon  after  the  premature  contraction  that  the  latter  is  still  in  the 
refractory  phase.  Ventricular  extrasystoles  may  occur  without  interfer- 
ing with  any  of  the  normal  stimuli,  in  which  case  the  pause  after  the  pre- 
mature contraction  is  shorter  than  normal,  and  an  "interpolated"  extra- 
systole occurs.     Inspection  of  the  phlebogram  shows  the  absence  of  an 


172 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


"a"  wave  to  correspond  with  the  extra  "c"  wave;  and  auscultation  of 
the  precordium  often  demonstrates  the  absence  of  a  second  sound  to  cor- 
respond with  the  ventricular  contraction. 

Auricular  extrasystoles  are  due  to  stimuli  arising  at  some  point  of 
the  auricle  other  than  at  the  sinus  node.  The  phlebogram  shows  an  "a" 
wave  preceding  each  extrasystole  of  the  ventricle.  The  compensatory 
pause  is  generally  absent,  but  may  be  almost  or  even  wholly  complete. 
Auricular  extrasj^stoles  may  be  induced  or  abated  by  digitalis. 

The  significance  of  extrasystoles  is  very  variable.  They  may  be  due 
to  many  direct  or  reflex  causes.  Thus  the  excessive  use  of  tobacco  may 
produce  them,  as  may  increased  blood-pressure,  especially  with  a  weak- 
ened myocardium. 


Fig.  141. — Coupled  beats.  The  coupling  is  visible  in  the  jugular  and  apex  tracings, 
only  occasionally  in  the  radial.  The  case  was  one  of  auricular  fibrillation  under  full  digi- 
talization.  The  radial  pulse  rate  is  about  one-half  of  that  of  the  heart.  An  extrasystole 
occurred  at  "x." 


PAROXYSMAL  TACHYCARDIA 

This  term  is  applied  to  a  distinct  pathologic  entity  due  to  a  disturb- 
ance of  the  intrinsic  cardiac  mechanism.  It  should  not  be  applied  to 
simple  tachycardia  clue  to  extrinsic  causes  such  as  exophthalmic  goitre. 

Clinically  this  condition  is  characterized  by  sudden  attacks  of  rapid 
heart  action  in  which  the  previous  cardiac  rate  is  approximately  doubled, 
trebled  or  quadrupled.  Ordinary  tachycardia  rarely  produces  a  pulse 
rate  over  140  per  minute,  in  paroxysmal  tachycardia  the  rate  ranges 
between  140  and  280  per  minute.  These  attacks  may  be  precipitated  by 
diverse  causes  such  as  excitement,  change  of  posture,  flatulence,  exercise, 
etc. ;  and  end  after  a  variable  duration  as  abruptly  as  they  began.  They 
are  frequently  associated  with  subjective  sensations  of  palpitation,  op- 
pression, fullness  of  the  neck,  dyspnea,  vertigo,  etc.,  the  intensity  of 
which  often  depends  upon  the  integrity  of  the  heart  muscle. 

Venous  and  electrocardiographic  studies  taken  at  the  beginning  and 
end  of  the  paroxysms  have  shown  that  the  cardiac  rhythm  may  be  vari- 
able.    Two  types  of  this  phenomenon  have  been  described: 

1.  The  type  in  which  the  auricular  type  of  venous  pulse  persists,  in 


CARDIAC    ARRHYTHMIA  173 

which  the  end  of  the  attack  may  terminate  with  normal  coordination 
or  with  a  temporary  auriculo-ventricular  block. 

2.  A  second  rarer  ventricular  type  has  also  been  observed  in  which 
the  paroxysms  are  characterized  by  the  entire  absence  of  auricular  waves, 
which  do,  however,  reappear  at  the  end  of  the  attack,  without  any  evi- 
dences of  auriculo-ventricular  block. 

The  etiology  of  paroxysmal  tachycardia  is  obscure.  Numerous  ex- 
planations such  as  the  interpolation  of  extrasystoles,  abnormal  stimulus 
production  in  the  Purkinje  cells  of  the  auriculo-ventricular  bundle,  etc., 
have  been  suggested.  Practically  the  condition  may  be  regarded  as  due 
to  an  increased  irritability  of  the  myocardium  in  which  diverse  reflex 
stimuli  may  precipitate  a  paroxysm. 

The  effects  upon  the  circulation  are  those  of  a  shortened  diastole  with 
insufficient  ventricular  filling,  as  the  result  of  which  arterial  pressure  falls, 
venous  pressure  rises  and  variable  degrees  of  local  or  general  circulatory 
stasis  may  occur. 

AURICULAR  FLUTTER 

Auricular  nutter  is  a  not  uncommon  form  of  arrhythmia  wmich  occurs 
chiefly  in  elderly  subjects.  It  is  characterized  by  an  extremely  rapid 
auricular  action,  the  rate  being  from  200  to  400  per  minute  (usually 
above  300).  When  established  it  generally  lasts  for  months  or  years, 
but  paroxysms  may  be  shorter.  It  is  due  to  pathologic  or  heterogenetic 
impulses  which  probably  have  an  ectopic  -auricular  origin.  It  is  not 
under  nerve  control.  The  rate  is  wonderfully  constant  as  a  rule,  and  is 
uninfluenced  by  position,  exercise  or  stimulation.  The  ventricular  rate  is 
generally  one-half  the  auricular  rate,  but  any  degree  of  block  may  be 
present.  The  ventricle  may  beat  regularly  if  the  degree  of  partial  block 
is  constant,  or  irregularly,  if  the  degree  of  block  varies  (e.g.,  3  to  2,  2  to 
1,  etc.).  Auricular  flutter  is  closely  related  to  paroxysmal  tachycardia. 
It  is  much  influenced  by  digitalis  and  vagal  compression.  Digitalis  may 
change  auricular  flutter  to  fibrillation  and  the  latter  to  a  normal  rhythm 
or  it  may  have  no  demonstrable  effect.  The  arterial  tracings  may  be 
regular  or  irregular,  fast  or  slow,  and  may  suggest  fibrillation  or  extra- 
systoles.  The  venous  curves  are  generally  obscure  on  account  of 
auricular  weakness,  but  when  pauses  are  long  "a"  waves  may  be  distinct 
(T.  Lewis).1 

AURICULAR  FIBRILLATION 

This  common  form  of  arrhythmia  occurs  in  serious  oiganic  lesions  of 
the  heart  muscle.  It  can  be  produced  experimentally  by  electric  over- 
stimulation of  the  auricle  and  may  be  regarded  as  manifestation  of 
auricular  exhaustion.  It  occurs  mainly  in  rheumatic  endocardial  lesions, 
especially  in  long  standing  mitral  stenosis  with  right  auricular  dilatation, 
but  is  also  seen  in  arterio-sclerotic  lesions.  It  is  identical  with  what  was 
formerly  described  as  "pulsus  irregularis  perpetuus,"  "nodal  rhythm" 
and  "delirium  cordis."  It  is  characterized  by  an  absolutely  irregular 
arterial  pulse.  The  pulse  waves  are  irregular  both  as  to  force  and  time, 
and  many  ventricular  contractions  fail  to  produce  a  peripheral  pulse, 

1  Lewis:  "Heart,"  IV,  1912,  171. 


174 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


hence  we  find  a  "pulse  deficit''  in  the  radial  and  other  peripheral  arteries. 
The  phlebogram  shows  the  absence  of  "a"  waves  and  the  presence  of  a 
large  "v"  wave,  which  can  also  often  be  seen  as  a  systolic  venous  pulsa- 
tion in  the  jugular  veins.  The  foregoing  characteristics  are  due  to  the 
fact  that  the  ventricle  instead  of  receiving  the  normal  stimuli  from  the 
sinus  node  transmitted  through  the  auriculo-ventricular  bundle  at  regular 
intervals,  and  with  definite  intermissions,  is  overwhelmed  by  stimuli 
received  so  frequently  that  diastolic  filling  and  rest  are  impossible. 
Digitalis  in  sufficient  dosage  produces  a  specific  reaction  which  is  attended 
by  excellent  clinical  results.  This  is  accomplished  by  lowering  the  con- 
ductivity of  the  auricular-ventricular  bundle,  so  that  fewer  stimuli  reach 
the  ventricle.  Excessive  dig  Utilization  often  results  in  the  production 
of  a  bigeminal  pulse  (p.  141).  A  rare  form  of  auricular  fibrillation  exists 
in  which  attacks  occur  in  paroxysms  lasting  a  few  hours,  days  or  weeks. 
They  may  be  brought  on  by  emotion  or  physical  strain,  and  may  cause 
severe  symptoms  of  cardiac  distress  and  palpitation.  Auricular  fibrilla- 
tion is  a  serious  form  of  arrhythmia  which  once  it  has  set  in  generally 
persists,  although  life  under  restricted  conditions  may  last  several  years. 


ajjuljliuuljlujljuuliu^ 


Fig.  142. — Auricular  fibrillation  showing  absolute  irregularity  of  the  brachial  pulse  with 
a  deficit,  as  contrasted  with  the  phlebogram.  The  latter  shows  an  absence  of  "a"  waves 
and  is  of  the  positive  or  ventricular  type.  From  a  case  of  broken  compensation  occurring 
in  rheumatic  mitral  and  tricuspid  disease. 

Blood-pressure  in  auricular  fibrillation  often  cannot  be  estimated  by 
the  usual  methods,  owing  to  the  variable  size  and  force  of  succeeding 
pulse  waves.  This  difficulty  may  be  overcome  by  the  method  suggested 
by  James  and  Hart : 

"The  apex  and  radial  impulses  are  counted  for  one  minute,  then  a 
blood-pressure  cuff  is  applied  to  the  arm,  and  the  pressure  raised  until 
the  radial  pulse  is  completely  obliterated;  the  pressure  is  then  lowered 
10  mm.  and  held  at  this  point  for  one  minute  while  the  radial  pulse  is 
counted;  the  pressure  is  again  lowered  10  mm.  and  a  second  radial  count 
is  made;  this  count  is  repeated  at  intervals  of  10  mm.  lowered  pressure 
until  the  cuff  pressure  is  insufficient  to  cut  off  any  of  the  radial  waves 
(between  each  estimation  the  pressure  on  the  arm  should  be  lowered  to  0). 
From  the  figures  thus  obtained  the  average  systolic  blood-pressure  is 
calculated  by  multiplying  the  number  of  radial  beats  by  the  pressures 
under  which  they  came  through,  adding  together  these  products  and 


CARDIAC    ARRHYTHMIA  175 

dividing  their  sum  by  the  number  of  apex  beats  per  minute.  The  result- 
ing figure  is  what  we  have  called  the  'average  systolic  blood-pressure.' ': 
The  following  observation  made  on  a  patient  will  indicate  the  method  of 
computation : 

B.  S.,  April  29,  1910.     Apex,  131;  radial,  101;  deficit, 30. 

Brachial  pressure  Radial  count 

100  mm 0 

90  mm 13       13  X  90  =  1,170 

80  mm 47  -  13  =  34  X  80  =  2,720 

70  mm 75  -  47  ^  28  X  70  =  1,960 

60  mm 82  -  75  =  7  X  60  =   420 

50  mm 101  -  82  =  19  X  50  =      950 

Apex  =  131)  7,220 

Average  systolic  blood-pressure 55  + 

PULSUS  ALTERNANS 

Pulsus  alternans,  the  third  in  order  of  frequency  and  prognostically 
one  of  the  most  grave  forms  of  cardiac  arrhythmia,  is  characterized  by  the 
alternate  appearance  of  large  and  small  arterial  pulse  waves.  The  time 
interval  separating  the  large  from  the  small  beats  is  generally  greater 
than  that  which  separates  the  small  waves  from  the  large  ones.  This 
form  of  arrhythmia,  which  can  be  produced  experimentally  after  ligation 
of  a  coronary  artery  if  the  heart  rate  is  much  increased,  is  due  to  failure 
of  ventricular  contractility  and  may  occur  (1)  in  a  normal  heart  beating 
at  an  excessive  rate;  or  (2)  in  a. degenerated  myocardium  contracting  at 
a  normal  rate.  The  rate  being  too  rapid  for  the  myocardium,  only  a 
partial  systole  occurs,  since  the  ventricle  is  insufficiently  rested,  but  in 
the  weaker  systole  less  energy  is  consumed  and  hence  the  next  contrac- 
tion will  be  normal  in  force.  According  to  another  explanation,  a  part 
of  the  ventricle  altogether  fails  to  contract,  remaining  in  a  refractory  state 
and  thus  causing  a  weak  contraction.  Whether  this  is  due  to  a  disturb- 
ance of  irritability,  conductivity,  or  contractility  is  still  an  open  question. 
The  last-mentioned  function  seems  to  be  most  commonly  at  fault. 
Gravier,  who  has  published  an  elaborate  monograph  on  the  subject, 
speaks  of  pulsus  alternans  as  "a  disorder  of  the  refractory  phase."1 

The  alternation  of  force  so  apparent  at  the  wrist  is  rarely  demon- 
strable at  the  cardiac  apex  and  the  relationship  has  actually  been  found 
reversed — a  strong  systole  being  associated  with  a  small  radial  pulse 
and  vice  versa.  The  explanation  of  this  phenomenon  perhaps  lies  in  the 
fact  stated  by  Hering  that  that  part  of  the  cardiac  musculature  which 
forms  the  cardiac  apex  is  not  the  part  which  propels  the  ventricular  blood 
into  the  aorta. 

Lewis  has  noted  a  similar  divergence  in  force  between  the  ventricle 
and  the  carotid,  which  he  attributes  to  alternating  auricular  force.  This 
corresponds  with  Volhard's  tracings  which  showed  an  alternation  of  the 
"a"  waves  in  the  phlebogram,  the  large  jugular  wave  being  followed  by 
the  small  radial  pulse. 

"Temporary  exhaustion  of  contractility  often  occurs  with  the  pro- 
duction of  a  typical  pulsus  alternans  from  an  overtaxation  of  the  cardiac 
musculature,  the  result  of  a  too  rapid  rate,  such  as  may  occur  in  paroxys- 

1  Gravier,  L. :  "L'Alternance  du  Coeur,"  Paris,  1914. 


176 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


mal  tachycardia,  auricular  flutter,  auricular  fibrillation,  or  the  long- 
continued  tachycardia  which  accompanies  Graves'  disease.  Experi- 
mentally it  may  be  produced  in  healthy  hearts  by  electrical  stimulation, 
the  injection  into  the  blood  stream  of  digitalis,  antiarin,  aconitin,  and 
hemolytic  serum.  It  is  most  frequently  encountered,  however,  when  the 
heart  is  beating  within  its  normal  rate,  and  when  it  denotes  a  grave 
pathological  condition  of  the  myocardium,  with  failing  contractility" 
(Gordinier). 

Pulsus  alternans  is  met  with  in  cases  of  nephritis  and  myocarditis, 
generally  during  failing  compensation.  It  may  be  complicated  by 
extr  asystoles. 

Pulsus  alternans  must  be  differentiated  from  regular  bigeminus  due 
to  extrasystoles.  The  latter  are  to  be  distinguished  from  true  alter- 
nans by  the  long  diastolic  time  interval,  or  by  the  long  compensatory 


£fe     <*7 


Fig.  143. — Pulsus  Alternans  from  a  case  of  cardio-vascular  sclerosis  with  angina  pec- 
toris. This  arrhythmia  was  apparently  precipitated  by  digitalis.  It  was  most  marked 
when  blood-pressure  was  at  its  highest  (S.  190,  D.  140  mm.  Hg.).  Death  three  months 
later.     Note  the  alternate  large  and  small  brachial  waves  occurring  at  regular  intervals. 


pause  following  the  small  extrasystolic  beats,  whereas  in  true  pulsus 
alternans  the  longer  period  follows  the  large  beat,  or  else  the  contractions 
are  equally  spaced  (Gordinier). 

The  phlebogram  in  pulsus  alternans  shows  no  abnormal  waves,  but 
the  "a-c"  interval  may  be  prolonged.  Alternation  in  the  intensity, 
quality  or  pitch  of  the  heart  sounds  is  rarely  demonstrable.  A  markedly 
dicrotic  pulse  may  on  superficial  inspection  simulate  alternation,  but  this 
source  of  error  may  readily  be  excluded  by  counting  the  pulse  over  the 
precordium.  Alternation  is  frequently  overlooked  if  sphj^gmographic 
tracings  are  not  made.  The  sphygmograph  is  also  useful  in  demonstrat- 
ing latent  cases  of  alternation.  It  also  enhances  one's  tactile  perception 
of  this  arrhythmia.  "The  cuff  is  inflated  to  the  point  at  which  the  pulse 
rate  becomes  halved.  If  the  cuff  pressure  is  allowed  to  fall  somewhat 
lower  all  the  beats  will  come  through,  but  the  alternation  in  their  size  be- 
comes more  noticeable  than  when  the  arterial  lumen  is  uncompromised."1 

1  Norms,  G.  W. :  "Blood-pressure,  Its  Clinical  Applications,"  Philadelphia,  1916, 
p.  243. 


CARDIAC    ARRHYTHMIA  177 

THE  "SOLDIER'S  HEART" 

The  symptoms  designated  by  the  term  "soldier's  heart"  consist  of 
dyspnea  on  exertion,  a  rapid  and  labile  pulse,  a  sense  of  exhaustion,  palpi- 
tation or  precordial  distress  and  vasomotor  ataxia.  Arterial  and  psychic 
hypertension  may  be  associated.  The  physical  signs  consist  of  enlarge- 
ment of  the  percussion  dulness,  variable  systolic  murmurs  and  sometimes 
arrhythmia. 

It  is  questionable  whether  we  are  dealing  with  a  definite  pathologic 
entity  or  simply  with  functionally  subnormal  hearts  whose  possessors 
have  suffered  from  extreme  excitement,  loss  of  sleep,  privation  and 
physical  strain,  together  with  the  excessive  use  of  tobacco,  coffee,  tea  or 
hypnotics.  Undoubtedly  many  cases  belong  to  the  last-named  class, 
but  it  seems  that  others  are  the  result  of  hyperthyroidism  or  toxic 
processes,  possibly  infections.  Psychic  factors  appear  to  play  a  role 
both  in  etiology  and  treatment,  but  in  a  considerable  number  of  cases 
the  damage  seems  to  be  permanent  so  that  the  cause  must  lie  deeper. 
The  "soldier's  heart,"  which  was  first  described  during  our  Civil  War, 
has  been  very  much  in  evidence  during  the  present  European  catastrophe 
(see  p.  191). 

THE  ESTIMATION  OF  VASOMOTOR  EFFICIENCY 

Many  tests  based  upon  sphygmographic  or  sphygmanometric  ob- 
servations for  the  determination  of  cardio-vascular  efficiency  have  been 
devised.  Thus  far  no  one  is  free  from  criticism,  or  entirely  satisfactory, 
but  the  following  test  which  is  simple  and  can  be  briefly  completed,  often 
sheds  a  useful  light  upon  doubtful  cases.  It  must  be  remembered,  how- 
ever, that  it  simply  aims  to  show  functional  efficiency,  not  structural 
integrity. 

Crampton's  Test  of  Vasomotor  Efficiency. — In  rising  from  the  re- 
cumbent to  the  erect  posture  blood-pressure  tends  to  fall  as  a  result  of 
gravity.  Unless  this  tendency  were  automatically  regulated,  syncope 
would  occur  as  a  result  of  cerebral  anemia.  In  a  normal  vigorous  man, 
however,  such  a  change  of  position  causes  a  rise  of  blood-pressure  amount- 
ing to  8  or  10  mm.  Hg.  This  increase  may  result  from  increased  vaso- 
motor tone  or  from  increased  cardiac  work,  or  as  a  result  of  both  factors. 
Bearing  these  facts  in  mind  Crampton1  has  devised  the  following  table 
to  test  vasomotor  efficiency  through  the  observation  of  pulse  rate  and 
blood-pressure  responses  to  postural  change.  The  tables  while  setting 
what  is  perhaps  a  high  normal  have  shown  that  vasomotor  tone  in  the 
same  individual  varies  greatly  as  a  result  of  mental  or  physical  fatigue, 
infectious  processes,  etc.  It  may  be  used  with  especial  edification  in 
the  study  of  essential  hypotension  cases. 

The  Technique. — The  cuff  of  the  sphygmomanometer  is  adjusted  over 
the  brachial  artery  and  the  patient  is  placed  on  a  comfortable  couch  with  a 
low  pillow.  The  heart  rate  is  counted  by  quarter-minutes  and  a  gradually 
decreasing  rate  is  usually  observed.  Counting  should  continue  until 
two  successive  quarter-minutes  are  the  same,  this  is  multiplied  by  4  and 
recorded.  The  systolic  pressure  is  then  taken  preferably  by  ausculta- 
tion.    The  patient  stands,  the  heart  rate  is  counted  as  before  until  it 

1  Crampton,  C.  W. :  "The  Blood  Ptosis  Test  and  Its  Use  in  Experimental  Work  in 
Hygiene,"     Proceed.  Soc.  Exp.  Biol.  &  Med.,  1915,  xii,  119. 
12 


178 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


reaches  the  "standing  normal,"  when  it  is  recorded,  and  the  blood- 
pressure  is  then  taken.  The  differences  are  calculated  and  reference  is 
made  to  the  scale. 

PERCENTAGE  SCALE 

Vasomotor  Tone 


Blood-pressure 

Heart-rate 

" 

increase 

+  10 

+  8 

+  6 

+  4 

+  2 

0 

-  2 

-  4 

-  6 

-  8 

-  10 

0  to  4 

100 

95 

90 

85 

80 

75 

70 

65 

60 

55 

50 

5  to  8 

95 

90 

85 

80 

75 

70 

65 

60 

55 

50 

45 

9  to  12 

90 

85 

80 

75 

70 

65 

60 

55 

50 

45 

40 

13  to  16 

85 

80 

75 

70 

65 

60 

55 

50 

45 

40 

35 

17  to  20 

80 

75 

70 

65 

60 

55 

50 

45 

40 

35 

30 

21  to  24 

75 

70 

65 

60 

55 

50 

45 

40 

35 

30 

25 

25  to  28 

70 

65 

60 

55 

50 

45 

40 

35 

30 

25 

20 

29  to  32 

65 

60 

55 

50 

45 

40 

35 

30 

25 

20 

15 

33  to  36 

60 

55 

50 

45 

40 

35 

30 

25 

20 

15 

10 

37  to  40 

55 

50 

45 

40 

35 

30 

25 

20 

15 

10 

5 

41  to  44 

50 

45 

40 

35 

30 

25 

20 

15 

10 

5 

0 

Note. — In  case  of  increase  in  pressure  higher  than  +10  add  3  per  cent,  to  the 
+  10  column  for  each  2  mm.  in  excess  of  10. 

"This  scale  provides  a  convenient  and  intelligible  method  of  record- 
ing and  reporting  cases  and  permits  a  numerical  statement  of  the  func- 
tion in  question.  Its  100  mark  indicates  a  perfectly  efficient  working 
of  the  vasomotor  system  under  test,  the  zero  is  approximately  the  point 
where  the  average, person  is  unable  to  maintain  the  erect  posture." 


CHAPTER  XVI 

THE  ELECTROCARDIOGRAPH 

By  Edward  B.  Krumbhaar,  Ph.  D.,  M.  D. 

Among  the  instruments  of  precision  recently  become  available  for 
clinical  purposes  is  the  electrocardiograph,  adapted  from  Einthoven's 
string  galvanometer.  In  the  short  space  of  time  elapsed  since  its  inven- 
tion in  1903,  it  has  not  only  already  proved  its  clinical  value  as  the  most 
accurate  analyzer  of  cardiac  arrhythmias,  but  bids  fair  to  give  informa- 
tion about  the  cardiac  muscle  that  is  obtainable  in  no  other  way.  In 
the  hands  of  Lewis,  Rothberger  and  Winterberg,  Kraus  and  Nicolai 
and  others,  it  has  materially  aided  in  increasing  our  knowledge  of  the 
mechanism  of  the  heart  beat,  both  in  health  and  disease. 


Fig.  144. — An  electrocardiograph  station.  A,  string  galvanometer;  B,  registering  ap- 
paratus (camera);  C,  electric  light;  D,  rheostat;  E,  leads  from  which  current  is  taken. 
{After  Hoffman.) 

The  Principle. — The  string  galvanometer  depends  on  the  principle 
that  a  conducting  string  or  wire  lying  in  a  strong  magnetic  field,  if  suffi- 
ciently sensitive,  will  move  vertically  to  the  lines  of  force  when  a  current 
passes  through  it.  As  every  contracting  muscle  initiates  such  a  current 
(the  part  at  which  the  contraction  starts  becoming  electrically  negative 
to  the  rest  of  the  muscle),  the  contractions  of  the  various  chambers  of  the 
heart  cause  a  series  of  such  deflections.     These  minute  currents  radiating 

179 


180  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

through  the  body,  if  the  extremities  of  the  patient  are  connected  with  the 
galvanometer  by  suitable  non-polarizable  electrodes,  may  be  perpetuated 
as  a  graphic  record  by  photographing  the  shadow  cast  by  the  vibrating 
string  on  a  moving  sensitive  film  or  plate.  The  galvanometer  and  regis- 
tering apparatus  are  so  arranged  that  a  contraction  starting  nearer  the 
base  of  the  heart  and  proceeding  toward  the  apex  will  cause  a  deflection  of 
the  vertical  string  to  the  left,  or  upward  on  standardized  records.  The  field 
of  the  electrocardiograph  and  its  limitations  will  be  best  comprehended,  if 
it  is  remembered  that  it  merely  registers  all  changes  of  electrical  potential 
occurring  between  the  two  electrodes  in  use.  Voluntary  muscle  tremors 
or  contractions,  when  present,  are  consequently  recorded  as  well  as  the 
heart  beat. 

The  three  leads  (places  for  attachment  of  electrodes),  adopted  by 
Einthoven  as  best  exhibiting  the  electrical  changes  caused  by  the  heart 
beat,  are  as  follows:  lead  I,  right  arm  to  left  arm  (horizontal);  lead  II, 
right  arm  to  left  leg  (long  axis  of  the  heart) ;  and  lead  III,  left  arm  to  left 
leg  (vertical).  These  leads  have  now  come  into  general  use,  and  should 
always  be  taken  in  routine  examinations.  Leads  may  be  taken  in  special 
cases,  however,  from  any  part  of  the  body.  A  time  marker,  registering 
fifths  or  twenty-fifths  of  seconds,  allows  an  accurate  computation  of  the 
various  time  intervals. 

The  Normal  Electrocardiogram.- — The  normal  mammalian  electro- 
cardiogram consists  of  a  single  summit  or  peak  ("P"  wave),  due  to 
contraction  of  the  auricles,  and  two  to  four  deviations  ("Q, "  "R," 
"S,"  "T"),  due  to  contraction  of  the  ventricles.  Of  these  four,  "R" 
and  "  T  "  are  the  most  constant,  and  "  Q"  and  "  S  "  are  of  little  importance 
in  the  normal  record.  Though  no  two  normal  hearts  give  exactly  similar 
records,  the  individual  peculiarities  are  retained  with  remarkable  con- 
stancy as  long  as  the  heart  stays  normal.  Although  the  factors  that 
cause  the  individual  deviations  are  not  yet  clearly  understood,  certain 
explanations  are  generally  accepted.  Thus  the  monophasic  "P"  sum- 
mit is  unquestionably  due  to  the  impulse  starting  at  the  sinus  node  and 
spreading  through  both  auricles  toward  the  ventricle.  This  is  followed 
by  an  inactive  period,  normally  of  0.12  to  0.17  seconds,  called  the  "P-R" 
interval,  which  corresponds  to  the  "A-C"  interval  of  polygraphic  trac- 
ings. Most  of  this  delay  is  caused  by  the  passage  of  the  impulse  through 
Tawara's  node  and  the  bundle  of  His.  The  path  followed  by  the  con- 
traction stimulus  on  entering  the  ventricle  is  a  very  complex  one,  not 
lending  itself  to  simple  representation  by  such  deviations.  The  "R" 
deflection  was  formerly  considered  as  the  evidence  of  the  basifugal  stim- 
ulus conduction  in  the  ventricle.  In  those  cases  where  it  was  preceded 
by  "Q,"  it  was  assumed  that  the  impulse  has  first  been  distributed  to 
tissues  near  the  apex  and  that  the  predominating  influence  for  a  short 
period  was  basipetal  (Einthoven).  Later  experimental  and  clinical  investi- 
gations by  Thomas  Lewis,  Buchanan,  and  de  Boer  indicate  that  the  form 
of  the  "Q,"  "R,"  "S"  group  of  the  ventricular  complex  is  the  result  of 
the  algebraic  summation  of  the  opposing  influences  of  the  right  and  left 
ventricle,  in  other  words,  a  bigram  due  to  the  superposition  of  dextrogram 
on  levogram.  From  this  point  of  view  "Q"  in  lead  I  ("Qi")  of  the  human 
electrocardiogram  is  a  left  ventricular  effect,  in  lead  II  and  III  ("Q2"  and 
"Q3")  a  right  ventricular  effect.  Clinical  confirmation  of  this  conception 
is  found  in  the  prominent  "Q?."  and  "Q3"  of  infants'  electrocardiograms 


THE    ELECTROCARDIOGRAPH 


181 


(Kmmbhaar  and  Jeiiks).  "R2",  "R3"  and  "Si"  are  due  to  spread  of 
activity  in  the  left  ventricle;  "Ri",  "S2"  and  "S3"  to  spread  of  activity 
in  the  right  ventricle.  The  "U"  wave,  which  is  occasionally  seen  in  both 
normal  and  pathological  records,  is  unimportant  and  but  little,  under- 
stood.    It  is  taken  by  Hering  to  be  due  to  vasomotor  activity,  i.e.,  an 


Ejsssz 


Fig.  145. — Normal  electrocardiogram.  Taken  from  the  three  customary  leads.  Lead 
I.  right  arm  to  left  arm;  lead  II,  right  arm  to  left  foot;  lead  III,  left  arm  to  left  foot.  Note 
that  Ri  is  the  largest.  In  this,  as  in  all  illustrations,  1  cm.,  deflection  of  string  (i.e.,  five  of 
the  small  ruled  lines)  represents  a  change  in  potential  of  one  millivolt.  Time  record,  H 
second. 

angiogram.  In  the  isoelectric  period  preceding  "T,"  a  balance  is  main- 
tained by  the  whole  mass  of  the  heart  being  in  a  state  of  contraction.  The 
final  deflection,  "T,"  is  taken  by  some  authorities  as  an  indication  of  the 
driving  force  of  the  heart,  represented  by  the  circular  muscle  bands  at  the 
roots  of  the  great  arteries.  It  is  usually  upright  but  may  be  diphasic  or 
inverted.  In  lead  III  this  inversion  has  little  significance;  in  the  other 
two,  it  is  considered  by  some  to  have  bad  prognostic  significance.     In 


182 


THE    EXAMINATION    OF    CIECULATORY    SYSTEM 


some  cases,  however,  it  is  unquestionably  a  sign  of  digit  alization  of  the 
heart  (Cohn).  The  direction  of  the  "T"  wave  is  thought  by  some  au- 
thorities to  depend  on  the  relative  duration  of  activity  of  the  two  ventricles 
(upright  "T"  due  to  persistence  of  right  ventricle). 


j^A — Al1 


No.  89.2 
($- Second- 


Fig.  146. — Preponderance  of  right  ventricle.  Curves  from  the  three  leads  in  a  case  of 
mitral  stenosis,  associated  with  auricular  and  right  ventricular  hypertrophy.  In  the  ven- 
tricular complexes  Ri  is  almost  absent  and  Si  is  very  large,  whereas  Rs  is  considerably  larger 
than  R2.  ■  Note  the  unusually  large  P  of  auricular  hypertrophy.  The  black  background 
and  white  string  of  this  illustration  are  due  to  the  fact  that  it  is  taken  directly  on  sensitive 
paper.  In  this,  as  in  a  few  others  of  the  illustrations,  some  lines  have  been  reinforced  for 
purposes  of  reproduction.      The  magnification  of  the  string  shadow  is  less  than  in  Fig.  145. 

Preponderating  Ventricular  Hypertrophy. — In  hypertrophy  of  the 
heart,  the  actual  size  of  "S"  and  its  size  relative  to  "R"  assume  great 
importance.     Thus,  when  the  mass  of  the  right  ventricle  has  become  rel- 


THE    ELECTROCARDIOGRAPH 


183 


atively  larger  than  that  of  the  left,  "S"  is  extremely  prominent  in  lead  I, 
whereas  the  "R"  of  lead  III  becomes  larger  than  that  of  lead  II  (normally 
the  largest).  Conversely,  when  the  mass  of  the  left  ventricle  has  become 
relatively  larger  than  the  right,  as  in  some  cases  of  aortic,  arterial  or  cardio- 
renal  disease,  "S"  is  extremely  prominent  in  lead  III,  whereas  the  "R" 
of  lead  I  has  become  larger  than  the  "  R"  of  lead  II.     These  phenomena, 


S&£r§= 


ggSl 


W-. — ^ ~i? — ^^-zrr- 


f1  iif«# 


-i — It— it — it 


-fc — -fc — It — It 


rj?m 


S> 


Fig.  147. — Preponderance  of  the  left  ventricle.  Note  thatfti  is  here  higher" than  722, 
and  that  <S3  is  the  deepest  of  all.  This  case  also  shows  interesting  abnormal  complexes,  re- 
curring in  groups  of  four.  It  will  be  noticed  that  although  the  first  three  complexes  of  each 
group  are  rhythmical,  yet  the  corresponding  P  and  T  waves  of  each  group  show  con- 
stantly recurring  small  differences.  The  fourth  complex  is  always  premature,  most  prob- 
ably a  nodal  extrasystole,  and  the  whole  represents  a  recurring  "dislocation  of  the  pace- 
maker.' 

the  meaning  of  which  has  been  put  on  a  logical  basis  by  the  investigators 
previously  referred  to,  have  been  confirmed  by  experimental  and  post- 
mortem evidence,  and  are  considered  by  Lewis  as  the  most  reliable  means 
of  estimating  the  relative  size  of  the  two  ventricles.  Recent  clinical 
evidence  brought  forward  to  contradict  this  view  has  not  been  sustained, 
but  it  is  certain  at  least  that  the  form  of  the  electrocardiogram  is  slightly 
influenced  by  the  position  of  the  heart  in  the  body.  (Compare  the  changes 
in  form  of  the  ventricular  complex  in  deep  respiration  and  after  removal 
of  large  pleural  effusions.) 


184 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


THE   CARDIAC  ARRHYTHMIAS 

As  the  different  types  of  cardiac  arrhythmias  have  been  set  forth  in 
the  previous  chapter,  it  will  be  necessary  here  only  to  indicate  how  they 
are  manifested  in  the  electrocardiograph. 

Sinus  Arrhythmia. — In  sinus  arrhythmia,  the  auricular  summit  and 
the  ventricular  complexes  are  of  the  normal  supraventricular  form;  in 
other  words,  the  impulse  arises  at  the  normal  site  and  traverses  the  normal 
channels.  That  it  is  given  out  from  the  sinus,  however,  at  irregular 
intervals,  can  readily  be  determined  by  measuring  the  varying  intervals 
between  the  "P"  summits. 

Extrasystole. — Extrasystoles  or  premature  contractions  appear  in  the 
electrocardiogram  in  very  striking  guise.  The  ectopic  origin  of  the  con- 
traction is  shown  by  marked  changes  in  the  shape  of  the  deviations. 


— "  fo :-".'■_  ■ 

-:~n — '■ —  -----  -r       — -^R —      — 3^-—         ,  fn 

-p 

P                         -P                    T»                           T> 
t-                    *r                       -r                   T 

1    •aXcir^ct^ 

-.,- — :       ,,     ••- 

*■    *    "  i1^    "  *     i"1  ■**— *    "A-1.  'V   ' <m^i^m^mimjmmlm 

Fig.  148. — Sinus  arrhythmia.  Note  that  although  all  complexes  are  of  normal  shape, 
and  the  P-R  interval  is  normal  and  constant,  yet  the  P  waves  occur  at  irregular  intervals, 
owing  to  arrhythmic  stimulus  production  in  the  sinus. 


Thus  in  auricular  extrasystole,  the  normal  "P"  either  becomes  flattened 
out,  diphasic  or  inverted.  It  is  usually  followed  by  a  normal  ventricular 
complex,  and  the  pause  is  very  rarely  compensatory.  Occasionally  an 
auricular  extrasystole  may  affect  the  succeeding  ventricular  complex, 
causing  a  so-called  "aberrant"  type.  This  may  vary  considerably  or 
only  slightly  from  the  normal  complex. 

Extrasystoles  arising  in  the  ventricle  have  been  grouped  into  three 
main  types,  according  to  the  site  of  origin.  All  are  easily  recogniz- 
able in  the  electrocardiogram  and  are  characterized  by  the  slowness  and 
great  amplitude  of  the  deflections.  Those  arising  near  the  apex  of  the 
left  ventricle  cause  in  lead  I  an  extremely  large  deflection  corresponding 
to  "R"  usually  with  an  inverted  "T";  in  lead  III,  the  deflection  corre- 
sponding to  "S"  is  unusually  deep  with  an  extra  large  "T."  Extrasys- 
toles arising  near  the  basal  portions  of  the  right  ventricle  cause  the  reverse 
of  this  picture  (i.e.,  deep  "S"  and  large  "T"  in  lead  I,  and  large  "R"  and 
inverted  "T"  in  lead  III).  The  site  of  origin  of  such  extrasystoles  has 
been  proved  by  stimulation  of  these  areas  in  animals  with  the  production 
of  similar  electrocardiograms.  Extrasystoles  arising  in  the  septum  or 
intermediate  positions  give  rise  to  a  variety  of  anomalous  complexes. 

Extrasystoles  arising  in  the  junctional  tissues  (Tawara's  Node  and 
His'  Bundle)  are  rare.     In  such  a  premature  contraction,  evidence  of 


THE     ELECTROCARDIOGRAPH 


185 


zt~Autf«c-KAir^ 


j&rZjtt 


-ft-Secr 


Fig.  149. — Auricular  extrasystole.  The  normal  rhythm  is  disturbed  by  the  premature 
appearance  of  a  P  wave.  In  such  cases  it  is  frequently  found  to  be  of  different  outline  than 
the  normal  or  inverted.  An  auricular  extrasystole  is  usually  followed  by  a  ventricular  com- 
plex of  normal  outline,  but  may  give  rise  to  an  "aberrant"  ventricular  complex,  as  in  the 
present  instance.  Note  the  larger  R  and  relatively  small  S  of  the  ventricular  complex.  The 
post-extrasystolic  pause  is  not  compensatory. 


&&*■,{    nHtjs^iM^ESMkt:! 


<fsM£: 


crfc 


Fig.  150. — Ventricular  extrasystole  arising  near  apex  of  left  ventricle.  The  deep  down- 
ward deflection  and  large  T  wave  indicate  that  this  extrasystole  arose  near  the  apex  of  the 
left  ventricle.  In  lead  III  it  would  probably  have  had  much  the  same  form,  and  in  lead  I, 
resembled  those  of  Fig.  154;  although  in  some  cases  the  form  remains  the  same  in  all  leads. 
Note  that  there  is  no  compensatory  pause  in  this  instance;  such  an  extrasystole  is  said  to  be 
"interpolated." 


Fig.  151. — Ventricular  extrasystole  arising  near  base  of  right  ventricle.  Note  the  ex- 
treme height  of  the  initial  deflection,  with  the  exaggerated  inverted  T.  The  deflection  time 
of  the  extrasystole  is  considerably  longer  than  the  normal.  The  extrasystolic  complex  in 
lead  III  was  identical  with  this,  whereas  in  lead  I  it  resembled  that  of  Fig.  153.  The  re- 
currence of  an  extrasystole  after  each  normal  beat  in  this  case  causes  a  true  bigeminy. 


186 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


auricular  activity  occurs  either  very  close  to  the  ventricular  complex 
(shortened  "P-R"  interval)  or  synchronously  with  the  ventricular  complex, 
which  is  of  the  normal  or  supraventricular  shape.  The  "P"  wave  is 
usually  diphasic  or  inverted  on  account  of  the  changed  direction  of  travel 
of  the  auricular  impulse. 

The  site  of  the  impulse  formation  of  the  premature  contraction  usu- 
ally remains  the  same  for  long  periods.  In  some  cases,  however,  the 
anomalous  impulse  may  arise  in  several  locations  ("  dislocation  of  the 
pacemaker").  (See  Fig.  C,  where  there  are  recurring  cycles  of  four  beats 
each.     The  stimulus  for  each  beat  of  the  four  arises  in  a  different  spot, 


•r — ___ 

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• 

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_J 

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"R 

■R 

vts-A' " 

T 

__,  --fr-  y^-f^ — *  A.  v- 

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~_«-U*lu/Vi-W* 

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V£fi(TRtCULAf% 

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A 

Fig.  152. — Ventricular  extrasystole  (intermediate).  Extrasystoles  arising  near  the 
ventricular  septum  appear  in  various  intermediate  forms,  such  as  seen  in  the  third  complex 
of  this  illustration.  Note  that  the  fundamental  auricular  rhythm  is  undisturbed.  The 
post-extrasystolic  pause  would  be  quite  compensatory,  were  it  not  for  the  fact  thatj  the  next 
succeeding  P-R  interval  is  shortened. 


Fig.  153. — Auricular  fibrillation.  From  a  case  of  rheumatic  mitral  disease  of  long 
duration.  Note  the  absence  of  P  waves  and  the  ventricular  arrhythmia.  The  irregular 
waves  of  fibrillation  occur  over  300  to  the  minute,  and  obscure  the  T  waves  of  the  ventricu- 
lar complex. 


the  last  of  the  four  being  a  nodal  extrasystole.)  If  for  any  reason,  the 
ventricular  rate  is  very  slow  (as  in  partial  block),  the  ventricle  may 
occasionally  "escape"  and  insert  a  beat  either  of  supra-  or  intraventricu- 
lar origin  into  the  otherwise  regular  rhythm. 

Auricular  Fibrillation. — Fibrillation  of  the  auricle  is  indicated  in  the 
electrocardiogram  by  three  phenomena;  first,  the  absence  of  "P,"  the 
sign  of  coordinate  auricular  contraction;  second,  the  presence  of  low, 
rapid  waves  of  fibrillation;  and  third,  the  irregular  response  of  the  ven- 
tricle. The  fibrillation  waves  are  best  detected  in  lead^  III,  or  by  a  special 
lead  from  sternum  to  vertebra?.  They  may  be  barely  discernible,  fine  or 
coarse.     The  ventricular  complex  is  of  supraventricular  type,  but  may 


THE    ELECTROCARDIOGRAPH 


187 


show  such  changes  as  those  found  in  ventricular  hypertrophy,  deficient 
conductivity  and  so  forth.  While  this  condition  is  usually  permanent, 
undoubted  cases  of  paroxysmal  or  temporary  fibrillation  have  been 
observed. 

Heart  Block. — The  various  stages  of  heart  block  are  easily  recogniz- 
able in  the  electrocardiogram.  In  the  earliest  stage  (delayed  conduc- 
tivity), the  time  interval  between  "P"  and"R"  is  found  to  exceed  the 
normal  limit  of  0.2  seconds.  In  the  next  stage,  " dropped  beat,"  the 
"P-R"  interval   gradually  gets  longer  and  longer  until   after  several 


R 


7R 


j^\**f^]#f\^^mm  j0*Aw%^" 


%       ::.:y   -- ■        -ri-:~.  '■;■ - 


Fig.  154. — Heart  block  A.  Prolonged  P-R  interval.  From  a  case  of  paroxysmal 
tachycardia^taken  between  paroxysms,  the  P-R  interval  is  prolonged  to  0.35  second.  At 
other  times,athe  P-R  interval  in  this  case  was  normal. 


Fig.  155. — Heart  block  B.  "Dropped  beat."  From  a  case  of  mitral  stenosis,  taken 
during  the  recurrence  of  acute  articular  rheumatism.  The  temporary  occurrence  of  partial 
heart  block  in  this  case  indicates  an  acute  rheumatic  myocarditis  of  the  junctional  tissues. 
With  subsidence  of  rheumatic  symptoms,  the  rhythm  returned  to  normal,  the  P-R  interval 
remaining  prolonged  for  several  days  after  the  dropped  beats  had  disappeared.  Note  here 
the  regular  recurrence  of  P,  the  gradual  increase  of  the  P-R  interval,  until  R  fails  to  respond, 
and  the  resulting  ventricular  arrhythmia.  In  spite  of  the  occasional  superposition  of  P  and 
T,  each  wave  can  usually  be  identified  by  measurement. 

beats,  a  second  "P"  follows  before  the  ventricle  has  responded  to 
the  first  auricular  impulse.  On  account  of  the  varying  "P-R"  interval, 
accurate  measurement  shows  a  ventricular  arrhythmia.  Dropped 
beats  may  occur,  however,  without  this  gradual  increase  of  the  "P-R" 
interval.  In  partial  block,  every  second,  third  or  fourth  "P"  (2  to  1, 
3  to  1,  or  4  to  1  block)  is  followed  by  the  ventricular  response.  In  3  to  2 
rhythm,  only  one  "P"  in  three  is  not  followed  by  ventricular  contraction. 
The  grades  of  block  may  change  from  moment  to  moment,  even  while  a 
record  is  being  made.  In  complete  block,  "  P  "  recurs  at  regular  intervals, 
but  bears  no  relation  to  the  much  slower,  but  also  regular  ventricular 
complex.  The  interpretation  of  these  records  is  sometimes  complicated 
by  the  coincidence  of  auricular  and  ventricular  contraction.  Careful 
analysis,  however,  of  the  summation  of  the  electrical  effects  thus  pro- 
duced will  show  evidence  of  each  of  the  individual  peaks. 


188 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


A  fairly  common  type  of  heart  block,  that  is  only  detectable  by  the 
electrocardiograph,  is  that  occurring  in  one  of  the  branches  of  His' 
Bundle.  If  one  or  other  is  deficient  in  conductivity,  an  anomalous  com- 
plex results,  which  resembles  that  of  right  or  left  ventricular  hypertrophy 
(q.v.),  except  that  the  deflection  time  is  considerably  lengthened,  and 
notching  of  the  "H"  peak  or  "S"  depression  is  frequent.  If  the  right 
branch  is  deficient  and  the  impulse  reaches  the  ventricle  through  the  left 
branch,  the  picture  resembles  that  of  left  ventricular  hypertrophy;  and 
vice  versa  if  the  left  branch  is  deficient.  This  condition  may  be  a  per- 
manent result  of  organic  disease  or  a  temporary  result  of  digitalis. 


fX^f^m^mm 


>EA2> 


x  Complete  B*-ock 


Fig.  156. — Heart  block  C.  Complete  block.  Note  that  the  P  wave  now  occurs  quite 
independently  of  the  ventricular  complexes,  i.e.,  there  is  no  simple  ratio  between  auricular 
and  ventricular  rate. 


BLJdK  iW^R^-r^Rftwfeir^p  Tfr%'  (Wj 


Fig.  157. — Heart  block  D.  Right  branch  of  His's  bundle.  From  a  case  of  decompen- 
sated myocarditis,  which  has  been  for  two  weeks  on  large  doses  of  digitalis.  Note  the 
notching  of  <S  and  the  prolonged  deflection  time  of  the  R—S  group  (more  than  0.1  second) . 
The  P—R  interval  is  prolonged  to  0.24  second.  As  both  these  signs  continued  after  the  ces- 
sation of  digitalis,  they  were  presumably  due  to  deficient  conductivity  caused  by  organic 
changes.''    Note  also  the  small  U  wave  that  is  occasionally  seen  in  normal  records. 


In  the  rare  condition  of  sino-auricular  block,  occasional  cycles  are 
entirely  absent  (i.e.,  there  is  no  evidence  of  either  auricular  or  ventricular 
activity).  It  is  assumed  in  these  cases  that  the  sinus  impulse  has  been 
blocked  before  reaching  the  auricle. 

Auricular  Flutter. — This  relatively  common  form  of  arrhythmia  was 
discovered  by  means  of  the  electrocardiograph,  and  it  is  still  impossible 
definitely  to  diagnose  the  condition  without  its  aid.  The  ectopic  origin 
in  the  auricle  of  the  rapid  stimulus  production  is  usually  shown  by  the 
inversion  of  "P"  in  one  or  other  lead.  If  due  allowance  is  made  for  the 
breaks  caused  by  "R"  and  "T,"  a  regular  rapid  succession  of  "P"  sum- 
mits can  be  traced  through  the  record.  As  the  ventricle  cannot  respond 
to  all  the  impulses  from  the  auricle,  a  state  of  partial  block  is  present.. 


THE    ELECTROCARDIOGRAPH 


189 


Fig.  158. — Auricular  flutter.  Curves  from  the  three  leads  of  a  case  of  persistent  auricu- 
lar flutter,  under  observation  for  over  two  years.  The  marked  ventricular  arrhythmia  is 
due  to  a  constantly  changing  degree  of  heart  block  (2:  1,  3:  1,  4:  1).  For  short  periods  a  3: 1 
block  with  regular  ventricular  rhythm  was  present.  The  auricular  rate  is  over  300,  the 
ventricular  about  120.  Time  intervals  of  2A  and  %s  second  are  recorded  by  heavy  and  light 
ventricular  lines. 


190 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


If  2  or  3  to  1,  the  ventricular  rhythm  will  be  regular;  if  a  3  to  2  rhythm 
exists,  the  ventricular  response  will  of  course  be  irregular.  This  ar- 
rhythmia with  the  distortion  of  the  succession  of  "P"  summits  by  the 
superposition  of  occasional  "T"  summits,  occasionally  makes  it 
difficult  to  diagnose  true  flutter  from  the  coarse  type  of  fibrillation. 

Pulsus  Alternans. — Many  cases  that  show  well-marked  alternation  in 
the  arteriogram  fail  to  show  any  abnormality  in  the  electrocardiogram; 
evidence  that  the  "R"  peak  is  not  a  measure  of  contractility.  Alterna- 
tion of  "R"  may  be  present,  however,  in  cases  that  may  or  may  not  show 
alternation  in  the  arteriogram.  This  might  be  taken  to  show  that  alterna- 
tion may  result  from  deficiency  in  irritability  or  stimulus  production  as 
well  as  in  contractility,  but  the  question  is  still  quite  undecided.  Con- 
siderable variation  may  occur  in  the  height  of  successive  "R"  waves, 
without  true  alternation  (e.g.,  the  changes  in  UR"  due  to  forced  respira- 
tion). If  the  respiratory  factor  can,  however,  be  excluded,  this  never 
occurs  in  the  normal  heart,  and  though  its  presence  is  not  necessarily  of 
grave  import,  it  must  be  taken  as  a  sign  of  myocardial  trouble.  Alterna- 
tion of  T  also  occurs. 


r->fecfc£jL»i/ '.  -^Sunv^o  ^sU^cm.^  .  •"t?«i*t  2/»4> . 


Fig.  159.- — Pulsus  alternans.  Taken  during  an  attack  of  paroxysmal  tachycardia. 
Note  the  alternating  height  of  R  (this  is  further  modified  by  changes  due  to  respiration). 
Note  also  in  each  cycle  that  the  bigger  R  is  associated  with  a  bigger  Q  and  a  smaller  <S. 
After  the  paroxysm  alternation  was  no  longer  found.  (N.B. — Alternation  may  also  cause  a 
similar  difference  in  height  of  the  T  waves.) 

Paroxysmal  Tachycardia.- — Electrocardiographic  records  taken  dur- 
ing a  paroxysm  of  paroxysmal  tachycardia,  frequently  show  only  two 
deflections,  "R"  and  a  combination  of  "T"  and  the  succeeding  "P:" 
If  these  are  separated,  however,  some  abnormality  in  "P"  usually  be- 
trays its  ectopic  origin  (inverted,  diphasic,  or  prolonged),  if  the  paroxysm 
is  of  auricular  origin.  In  some  paroxysms,  however,  if  the  new  site  of 
stimulus  production  is  near  the  sinus  node,  "P"  almost  or  entirely 
retains  its  normal  shape.  The  end  of  a  paroxysm  is  shown  by  the  sudden 
slowing  of  the  cardiac  rate,  with  the  appearance  of  a  normal  "P"  fol- 
lowed by  a  normal  ventricular  complex.  Occasionally  isolated  auricular 
extrasystoles  may  disturb  the  normal  rhythm  for  a  short  period  after  the 
end  of  the  paroxysm,  or  the  paroxysm  may  end  in  a  short  transition 
period  of  auricular  or  ventricular  fibrillation. 

Paroxysms  due  to  heterogenetic  impulses  arising  in  the  ventricular 
or  junctional  tissues  are  rare.  The  former  are  characterized  by  the  ano- 
malous form  of  the  ventricular  complex;  the  latter  by  the  very  short  or 
absent  "P-R"  interval. 

Combined   Arrhythmias. — A   combination  of  two  or  more  of  these 


THE    ELECTROCARDIOGRAPH 


191 


arrhythmias  may  occur  in  a  single  record.  Thus  in  cases  of  auricular 
fibrillation  the  dominant  complex  of  "supraventricular"  origin,  may 
occasionally  be  replaced  by  a  beat  of  "intraventricular"  origin,  indistin- 
guishable in  form  from  a  ventricular  extrasystole  or  premature  contrac- 
tion. In  the  coupled  beat  of  digitalis,  the  second  beat  of  each  pair  is  of 
this  character.  Just  as  the  ventricle  may  "escape"  if  its  irritability 
reaches  too  high  a  level,  so  the  impulse  from  an  auricular  extrasystole 
may  be  blocked  if  it  reaches  the  ventricle  when  its  irritability  is  still 
lowered  by  the  preceding  beat  (refractory  period).     An  example  of  this 


fiajcsfc 


Fig.  160. — Paroxysmal  tachycardia  (auricular).  Three  beats  of  the  paroxysm  are 
reproduced  to  the  left.  The  P-R  interval  is  prolonged  and  P  and  T  are  superimposed. 
The  rate  is  about  120;  the  rhythm  suddenly  drops  to  about  70,  the  P-R  interval  remaining 
prolonged.  When  the  P  waves  of  the  paroxysm  are  visible,  they  are  usually  found  to  be  of 
abnormal  shape  or  inverted. 


• 

•    •           ••• 

r  :    t—        .• — — — — 

••                      •••• 

ft 

-a 

»                   *                                      -r*                  'O 

■V- 

-■-                      m-            '   .'•                                       ./L1--L-J1                           •_..-»: 

V 

i      -p         c 

T              ?     -IvL                V        '  *¥       X     T> 

m^k^ 

V 

Y 

n      J               «:.  .  ■ 

tt 

/rsw. 

•S— A-A» 

•s^-/v^>- 

rf^^^B  r^w^^a^i  '■^i    ^    ^    <*•  -^     -^    -^     >V   ^V     .A    ^s.    ^V 

™               , 

Fig.  161. — Blocked  auricular  extrasystole.  The  norma!  rhythm  is  interrupted  by  a 
long  pause,  and  it  will  be  noted  that  the  T  wave  of  the  preceding  systole  is  altered  by  the 
superposition  of  the  auricular  extrasystole  (P1).  That  this  (and  not  sino-auricular  block) 
is  the  correct  interpretation,  is  confirmed  by  the  fact  that  the  alteration  of  the  T  wave  is 
constant,  and  that  after  the  administration  of  atropin,  the  auricular  premature  contraction 
is  invariably  followed  by  a  ventricular  contraction  which  partially  obliterates  the  pause. 


is  given  in  the  accompanying  figure,  which  duplicates  the  picture  of 
sino-auricular  block,  except  for  !the  fact  that  the  T  wave  preceding  the 
pause  is  altered  by  the  superposed  auriclar  extrasystole. 

The  "Soldier's  Heart." — In  regard  to  the  "soldier's  heart"  or  "ex- 
haustion heart,"  which  has  received  much  attention  in  the  present  war, 
the  electrocardiograph  furnishes  only  what  evidence  might  be  expected 
from  consideration  of  the  preceding  paragraphs.  Arrhythmia  when 
present  is  nearly  always  either  of  the  sinus  or  extrasystolic  type,  and 
disappears  with  the  recovery  of  the  patient.     The  signs  of  preponderance 


192  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

of  one  or  other  ventricle  (usually  the  right)  are  occasionally  found,  and 
some  cases  of  dilated  hearts  show  the  small  deflections  of  "R"  and  "S," 
such  as  are  often  associated  with  myocardial  weakness  (see  p.  177). 

CONCLUSION 

From  the  above  considerations,  it  will  readily  be  seen  that  much  of 
the  information  given  by  the  electrocardiograph  has  not  yet  been  prop- 
erly appraised.  In  the  analysis  of  cardiac  arrhythmias,  to  be  sure, 
most  moot  points  have  already  been  settled;  but  as  an  indicator  of  the 
condition  of  the  heart  muscle — the  most  important  item  in  the  prognosis 
and  treatment  of  cardiac  disease — the  limitations  and  possibilities  of  the 
electrocardiograph  have  not  yet  been  realized.  It  furnishes  valuable 
evidence  about  the  relative  size  of  the  two  ventricles,  locates  the  site  of 
origin  of  abnormal  stimuli  and  accurately  determines  the  various  time 
relations  of  the  cardiac  cycle.  Repeated  records  give  information  in 
several  ways  about  the  progress  of  the  disease  and  the  response  of  the 
heart  to  digitalis.  Like  all  other  clinical  instruments  of  precision,  how- 
ever, it  is  at  the  best  but  one  of  several  aids  to  the  discriminating 
physician. 


CHAPTER  XVII 
PALPATION 

THE   CARDIAC  IMPULSE 

This  term  is  applied  to  the  impulse  of  the  heart  against  the  chest  wall. 
The  study  of  this  phenomenon  may  be  carried  on  by  simple  inspection, 
by  palpation  or  by  graphic  records. 

The  occurrence  of  the  cardiac  impulse  marks  the  time  of:  (1) 
ventricular  contraction;  (2)  the  beginning  of  the  first  sound;  (3)  arterial 
filling.  It  is  felt  as  a  slight  movement  under  the  chest  wall,  somewhat 
gliding  and  slightly  lifting  in  character,  of  definite  rhythm  but  uncer- 
tain beginning,  whose  intensity  depends  on  (a)  the  rapidity  and  force  of 
the  ventricular  contraction,  but  even  more  largely  on  (6)  the  shape  of  the 


Fig.   162. — The  normal  cardiogram. 

chest — the  extent  to  which  the  lungs  overlap  the  heart;  and  finally  upon 
(c)  the  amount  and  character  of  overlying  soft  tissue.  Thus  in  deep- 
chested,  or  corpulent  individuals  and  in  recumbency,  the  impulse  may  be 
normally  imperceptible;  while  in  long-chested  persons,  especially  in 
emaciated  subjects,  in  children,  during  forced  expiration,  under  excite- 
ment, or  exertion,  it  is  disproportionately  strong.  The  point  of  percep- 
tion is  found  lower  by  palpation  than  by  inspection.  The  duration  of 
the  impulse  is  normally  about  one-third  of  a  second. 

During  ventricular  systole  the  heart  (1)  becomes  smaller,  especially 
in  its  transverse  diameter ;  (2)  twists  about  its  longitudinal  axis  from  left 
.to  right  and  forward  (Hirschf elder). 

It  has  been  graphically  shown  that  what  we  see  as  the  "apex  beat" 
consists  of  variable  and  often  complex  elevations  and  depressions  of  the 
precordium.     The  movements  may  be  grouped  as: 

1.  A  normal  type:  a  considerable  protrusion  of  the  precordium,  occur- 
ring with  and  during  ventricular  systole.  Graphic  tracings  in  such  a 
case  show  three  waves:  (a)  auricular  systole;  (b)  ventricular  systole;  (c) 
rebound  due  to  ventricular  diastole  (see  Fig.  129). 

2.  Elevation  of  the  whole  precordium  due  to  pivotal  action  of  the 
13  t193 


194 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


heart  against  the  vertebral  column.  Seen  chiefly  in  hypertrophied 
hearts,  especially  in  flat-chested  people. 

3.  Systolic  retraction. 

During  systole,  the  right  side  of  the  right  ventricle  tends  to  recede 
from  the  chest  wall.     When  this  chamber  is  hypertrophied  or  acting 


Fig.  163. — The  cardiac  impulse  ("apex  beat")  does  not  correspond  to  the  anatomic 
apex  of  the  heart  but  is  due  to  a  sudden  hardening  and  increase  in  tension  of  the  anterior 
surface  of  the  right  ventricle,  about  1  inch  (2.5  cm.)  to  the  right  of  the  anatomic  apex. 

Practically  the  whole  anterior  surface  of  the  heart,  is  the  right  heart.  The  left  ventricle 
normally  forms  only  the  extreme  left  border  of  the  anterior  surface  and  comes  in  contact 
with  the  chest  wall  mainly  when  this  chamber  is  enlarged,  as  is  the  case  in  the  accompany- 
ing photograph,  in  which  the  whole  heart,  but  especially  the  left  ventricle,  is  greatly  hyper- 
trophied. 


forcibly,  sufficient  negative  intrathoracic  pressure  is  produced  to  cause 
a  sinking  in  of  more  or  less  of  the  precordium.  This  normal  retraction 
is  sometimes  mistakenly  attributed  to  pericardial  adhesions.  When  both 
elevation  and  retraction  are  coincidentally  present  over  different  areas, 
we  get  an  impression  of  a  wavy  or  peristaltic  impulse.  Retraction,  else- 
where, may  be  caused  by  pericardial  adhesions  and  when  noted  posteriorly 


PALPATION  195 

at  the  level  of  the  eleventh  and  twelfth  ribs  is  known  as  BroadbenVs  sign 
of  adhesive  pericarditis. 

The  examination  of  the  cardiac  impulse  is  of  diagnostic  importance 
since  it  enables  us  to  estimate  the  degree  of  enlargement  or  displacement 
of  the  heart,  especially  to  the  left  and  downward,  and  often  to  determine 
whether  enlargement  is  due  to  hypertrophy  or  dilatation.  It  is  impor- 
tant, therefore,  to  know  not  so  much  the  point  of  maximum  intensity, 
but  the  lowermost,  outermost  point  of  impulse.  It  also  enables  us  to 
accurately  count  the  pulse  in  auricular  fibrillation,  etc.,  when  the  radial 
count  is  no  longer  a  criterion  of  the  pulse  rate.  It  also  renders  possible 
the  timing  of  heart  sounds,'  murmurs,  thrills,  etc. 


Fig.  164. — Palpation  of  the  precordium.  The  hand  should  rest  lightly  upon  the 
chest  wall  in  order  to  determine  the  position  and  character  of  the  cardiac  impulse,  or  the 
existence  of  thrills. 

Palpation  of  the  cardiac  impulse  is  generally  more  satisfactory  than 
mere  inspection.  By  placing  a  finger  tip  in  an  intercostal  space,  or  by 
laying  the  whole  palmar  surface  of  the  fingers  lightly  upon  the  pre- 
cordium we  not  only  confirm  the  data  obtained  by  inspection  but  we  may 
determine  other  important  phenomena.  In  left  ventricular  hypertrophy 
a  forcible,  deliberate,  prolonged  heaving  impulse  is  felt,  while  that  of 
dilatation  often  has  an  abrupt,  slapping  quality.  A  heaving  impulse, 
however,  may  be  noted  even  in  dilatation  when  compensation  is  far  from 
good.  The  force  of  the  impulse  is  decreased  in  obesity,  emphysema,  edema 
of  the  precordium,  thickening  of  the  lung  or  pleura,  feeble  heart  action, 
cardiac  dilatation,  pericardial  or  pleural  effusion. 

Pulsation  of  the  aorta  may  sometimes  be  noted  in  the  second  left 


196  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

intercostal  space,  but  when  marked  should  always  suggest  the  possibility 
of  aneurism  (Fig.  412).  The  pulsation  most  commonly  encountered  at 
the  base  of  the  heart  is  that  of  the  pulmonary  artery.  Epigastric  pulsation 
generally  indicates  active  right  ventricular  contraction  or  a  low  diaphragm. 
It  is,  therefore,  most  marked  when  this  chamber  is  hypertrophied,  or 
when  general  visceroptosis  is  marked.  Pulsation  in  this  region  may  result 
from  abdominal  aneurism,  tumor,  a  relaxed  aorta,  or  from  a  pulsating 
liver  (tricuspid  insufficiency).  A  diastolic  "shock"  over  the  base  of  the 
heart  indicates  a  sudden,  forcible  closure  of  the  semilunar  valves.  It 
may  be  felt  when  congestion  of  the  lungs  is  associated  with  a  vigorous 
right  heart,  and  in  aortic  aneurism. 

In  referring  to  the  apex  impulse  it  is  to  be  definitely  understood  we 
mean  the  outermost,  lowermost  point  at  which  it  is  either  visible  or  palpable, 
and  not  the  point  of  maximum  intensity.  It  is  generally  felt  as  a  diffuse 
throb  3±  inch  inside  the  left  border  of  percussion  dulness .;  and  almost  always 
one  interspace  higher  than  the  silhouette  obtained  by  the  orthodiagraph : 
firstly,  because  it  is  felt  and  seen  in  systole,  while  the  X-ray  shows  the 
heart  in  diastole  (Dietlen) ;  and  secondly,  because  what  is  generally  felt  as 
the  apex  beat  is  not  due  to  a  slapping  of  the  anatomic  apex  against  the 
thoracic  parietes,  but  to  a  sudden  marked  increase  in  tension  of  the  lower, 
anterior  surface  of  the  right  ventricle. 

The  left  ventricle  is  a  direct  factor  in  its  production  only  in  case  of 
hypertrophy  of  that  chamber,  or  of  cardiac  displacement.  "The  ana- 
tomic apex,  formed  by  the  tip  of  the  left  ventricle,  comes  into  direct  con- 
tact with  the  thoracic  wall  only  when  the  apex  is  situated  far  enough  to 
the  left  to  strike  the  lateral  wall  of  the  chest"  (Dayton).1 

Normal  Position  of  the  Cardiac  Impulse. — The  cardiac  impulse  is 
normally  observed  (in  adults)  in  the  fifth  interspace  slightly  within  the 
mid-clavicular  line  as  an  ill-defined  and  sometimes  distinctly  wavy  eleva- 
tion and  retraction  of  the  intercostal  space.  From  what  has  been  stated 
it  is  evident  that  the  position  and  character  of  the  cardiac  impulse  will 
vary  greatly  in  different  individuals.  Such  variations  may  result  from 
a  change  of  posture:  the  impulse  is  generally  less  marked  in  recumbency, 
and  can  often  only  be  felt  when  the  individual  is  erect  and  leans  forward ; 
sometimes  in  normal  cases  not  even  then.  The  assumption  of  the  left 
lateral  decubitus  causes  it  to  move  1^  to  2  inches  to  the  left;  lying  on 
the  right  side  causes  less  displacement.  The  failure  of  the  impulse  to 
move  with  a  change  of   posture  may  be  due  to   pericardial  adhesions 

1  Numerous  physiologists^teach  that  the  apex  impulse  is  due  to  the  thrust  of  the 
left  apex  against  the  chest  wall,  the  heart  being  rotated  on  its  axis  in  the  process  of 
contraction,  so  as  to  bring  the  left  ventricle  into  an  anterior  position.  In  defence  of 
the  statement  made  by  us  the  following  facts  may  be  mentioned:  (1)  The  left  ven- 
tricle in  the  normal  heart  is  a  posterior  structure,  only  a  narrow  margin  of  which  is 
visible  from  in  front.  (2)  The  cardiac  dulness  always  extends  at  least  \4,  inch  to  the 
left  of  the  outermost  portion  of  the  apex  impulse,  showing  that  the  impulse  is  not  pro- 
duced by  the  anatomic  apex  of  the  heart.  (3)  The  fact  that  the  exposed  heart  can  be 
seen  to  twist  upon  its  axis  during  systole  is  not  proof  that  the  normally  surrounded 
heart  performs  the  same  movement.  "The  heart  is  not  tilted  forward  to  the  right 
during  systole;  this  occurs  only  when  the  heart  has  been  displaced  on  opening  the 
chest."  (4)  "As  the  heart  expands  during  diastole  it  becomes  at  the  same  time  so 
flaccid  as  to  flatten  by  its  own  weight;  it  therefore  becomes  distorted  by  the  ever- 
changing  walls  of  the  cavity  in  which  it  rests  (chest  walls  and  lungs)  and  during 
systole  its  first  act  is  to  recover  itself,  'asserting  itself,  against  the  tissues  which  sur- 
round it.'  This  causes  the  apex  beat"  (Haycroft,  J.  B.:  "The  Movements  of  the 
Heart  within  the  Chest  Cavity  and  the  Cardiogram,"  Jour.  Physiol.,  1891,  438). 


PALPATION 


197 


(Figs.  218,  361,  362).  Excessive  motion  "cor  mobilis"  (3  to  5  inches)  oc- 
curs in  cardioptosis,  and  is  associated  with  a  low  diaphragm,  and  often 
with  visceroptosis  and  arterial  hypotension.  The  cardiac  impulse  is  higher 
in  children,  and  lower  in  old  age,  than  in  adult  life.  A  feeble  impulse,  like 
a  faint  heart  sound,  by  no  means  indicates  a  weak  heart  action.  It  points 
rather  to  large  lungs,  a  deep  chest  or  thickness  of  the  superficial  tissues. 

Trachea 


Right  bronchus 

Branch,  left  pul- 
monary artery 

Left  superior  pul- 
monary vein. 

Left  inferior  pul- 
monary vein 


Left  auricle 


Thoracic  aorta 


Plight  kidney 


Stomach 


Spleen 


Left  kidney 


Spinal  cord 

Fig.  165. — The  posterior  part  of  the  middle  mediastinum.  Showing  the  anatomic 
relations  immediately  behind  the  heart  viewed  from  in  front.  Compare  Figs.  91  and  92, 
showing  the  rear  view. 


Displacement  of  the  Cardiac  Impulse. — The  cardiac  impulse  may  be 
displaced  downward  if  the  diaphragm  occupies  a  low  position  (cardi- 
optosis, visceroptosis)  and  in  left  ventricular  hypertrophy.  It  may  be 
found  to  the  right  of  its  normal  position  in  pericardial  effusions,  left- 


198  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

sided  pleural  effusions  or  pneumothoraces,  or  as  a  result  of  right-sided 
pulmonary  adhesions  or  fibrosis,  as  well  as  in  situs  inversus  viscerum. 

' '  The  character  and  degree  of  cardiac  displacement  in  cases  of  peri- 
cardial effusion  depends  mainly  upon  the  degree  of  compensation — the 
degree  of  increased  venous  pressure — in  other  words  upon  the  specific 
gravity  of  the  heart.  If  venous  pressure  is  considerably  higher  than 
intrapericardial  pressure,  the  heart  will  contain  a  normal  amount  of 
blood  and  remain  in  its  normal  position;  if  venous  pressure  is  low,  the 
heart  will  contain  but  little  blood  and  hence  will  be  pushed  upward  and 
backward,  the  apex  deviating  to  the  right"1  (see  Figs.  358,  359,  360). 

It  may  be  displaced  to  the  left  in  hypertrophy  or  dilatation  of  the 
ventricles,  especially  the  left;  or  by  a  right-sided  pleural  effusion  or  pneumo- 
thorax and  as  a  result  of  left-sided  pulmonary  fibrosis. 

Dislocation  in  an  upward  direction  may  be  caused  by  a  high  dia- 
phragmatic position — meteorism,  ascites,  pregnancy,  massive  abdominal 
tumors — or  by  fibrosis  of  the  upper  pulmonary  lobes. 

THRILLS 

A  thrill  is  the  tactile  perception  of  vibrations  produced  by  flowing 
liquids.  It  generally  consists  of  intermittent  vibrations  of  the  chest  wall, 
not  unlike  the  sensation  imparted  by  a  purring  cat;  but  the  vibrations  of 
a  thrill  are  much  finer  and  more  rapid.  Experimentally  thrills  may  be 
produced  by  constricting  a  rubber  tube  or  a  blood-vessel  through  which 
fluid  is  flowing.  They  are  due  to  vibrations  of  tissues,  the  mechanism 
being  similar  to  that  which  produces  murmurs  (see  p.  221).  They  may 
disappear  if  blood  flow  is  insufficiently  rapid  to  throw  the  tissues  into 
vibration — low  pressure,  weak  heart.  Like  murmurs,  they  may  be  con- 
ducted by  the  blood  stream  or  the  vessel  walls.  "The  hand  must  be  placed 
very  lightly  upon  the  chest  wall,  since  firm  pressure  may  abolish  the 
vibrations,  which  are  generally  produced  by  the  eddies  in  the  blood  stream, 
caused  by  localized  constrictions  or  dilatations  of  the  heart  chambers  or 
vessel  walls,  e.g.,  mitral  obstruction,  aortic  aneurism. 

In  studying  a  thrill  it  is  essential  to  determine:  (1)  the  exact  time  of 
the  cardiac  cycle  at  which  it  occurs.  This  is  accomplished  by  noting  the 
relation  of  the  latter  to  the  apex  impulse,  (2)  the  location,  and  (3)  the 
extent  of  the  thrill. 

Normal  Thrills. — These  occur  when  heart  action  is  vigorous  and  the 
chest  wall  is  thin — children,  emaciated  subjects,  retracted  lungs.  In 
these  cases  the  first  heart  sound  is  often  loud  and  somewhat  rasping,  and 
in  children  the  pulmonic  second  sound,  loud.  These  signs  may  lead  to 
an  erroneous  diagnosis  of  mitral  obstruction,  especially  since  with  a 
rapid  heart  action  a  normal  systolic  thrill  may  be  interpreted  as  being 
presystolic,  and  inasmuch  as  a  normal  presystolic  sound  is  sometimes 
audible  (see  p.  215). 

Such  cases  may  be  differentiated  from  mitral  obstruction  by  the  fact 
that  in  the  latter  condition  the  heart  is  enlarged,  the  pulse  volume  small, 
the  rate  not  infrequently  irregular,  while  the  pulmonic  second  sound  is 
unduly  accentuated.  In  addition  to  these  signs  the  patient  with  a 
stenotic  lesion  is  apt  to  suffer  from  dyspnea,  cyanosis,  or  cough  on  severe 
exertion. 

1  Norris,  G.  W.:  "Studies  in  Cardiac  Pathology,"  1911,  123. 


PALPATION 


199 


Pathologic  Thrills. — Thrills  of  pathologic  origin  are  encountered  in 
valvular  heart  disease  and  in  aortic  aneurism.  Thrills  may  also  be  felt 
in  the  large  arteries  and  veins,  as  well  as  over  the  thyroid  gland  in  exoph- 


L.I.V. 


R.A.A 


R.V 


L.B. 


Fig.  166. — Section  through  the  middle  of  the  sternum  and  vertebral  column 
(adult).  Showing  the  anatomic  relations  of  various  cardiac  structures.  At  this  point  the 
heart  occupies  practically  the  entire  mediastinal  space.  The  esophagus  lies  closely  behind 
the  left  auricle.  Venous  tracing  depicting  the  functional  activity  may  be  made  by  intro- 
ducing a  rubber  capsule  into  the  esophagus.  T.,  trachea;  L.I.V.,  left  innominate  vein; 
R. A. A.,  right  auricular  appendage;  R.V.,  right  ventricle;  A.,  aorta;  R.P.A.,  right  pulmo- 
nary artery;  L.B.,  left  bronchus;  L.A.,  left  auricle;  R.A.,  right  auricle;  .4,  abdominal  aorta; 
V.C.,  inferior  vena  cava. 


thalmic  goitre.  The  most  intense  systolic  thrills  are  generally  met  with 
in  aortic  obstruction,  and  pulmonary  stenosis.  Very  marked  diastolic 
thrills  are  frequently  encountered  in  aortic  insufficiency  and  mitral 
obstruction. 


CHAPTER  XVIII 
PERCUSSION  OF  THE  HEART 

The  heart  is  outlined  by  percussion  in  order  to  determine:  (1)  the  size 
of  the  organ  as  a  whole  or  the  relative  size  of  its  different  chambers; 
(2)  its  position;  (3)  the  size  of  the  great  vessels  at  its  base. 

Method. — (1)  Begin  percussing  below  the  left  clavicle  and  continue 
downward  until  the  upper  border  of  cardiac  dulness  is  reached.     This 


R.V 


Fig.  167. — The  anterior  chest  wall  viewed  from  behind.  This,  the  first  of  a  series  of 
sections,  shows  the  anterior  wall  of  the  heart  viewed  from  within,  surrounded  by  the  lungs. 
R.V.,  anterior  wall  of  right  ventricle;  S,  stomach;  D,  diaphragm. 

point  is  indicated  by  a  diminution  of  pulmonary  resonance  and  will 
generally  correspond  to  the  upper  border  of  the  third  rib.  (2)  Percuss 
from  the  left  mid-axillary  line  toward  the  heart  and  note  the  point  at 
which,  over  different  ribs  or  interspaces  the  percussion  sound  becomes 

200 


PERCUSSION    OF    THE    HEART 


201 


Fig.  168. — Orthopercussion.  The  tendency  is  for  the  examiner  to  underestimate  the 
right,  and  overestimate  the  left,  border  of  the  heart.  The  latter  tendency  may  be  mini- 
mized by  using  ortho-percussion  with  a  very  light  stroke. 


Fig.  169. — Horizontal  section  through  the  chest.  Showing  the  unavoidable  margin  of 
error  in  outlining  the  left  cardiac  border  by  percussion.  The  solid  line  indicates  the  ver- 
tical penetration  of  the  orthodiagraph.  The  dotted  line  illustrates  the  oblique  penetration 
of  percussion  vibrations.  A-B,  orthodiagram  shadow.  A-C,  percussion  dulness.  Light 
vertical  percussion  (orthopercussion)  minimizes  lateral  radiation  and  gives  the  mosl  ac- 
curate results  attainable  by  percussion.  The  tendency  is  generally  to  overestimate  the 
left  and  to  underestimate  the  right  cardiac  border.  The  margin  of  error  is  increased  in 
cases  of  left  ventricular  enlargement  and  in  patients  with  deep  thoraces.  The  drawing 
further  shows  the  deep  situation  of  the  mitral,  and  the  relatively  superficial  position  of 
the  tricuspid  valves.      (After  Braune.) 


202 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


slightly  dull.     (3)  Percuss  from  the  right  mid-clavicular  line  and  outline 
the  right  border  in  a  similar  manner. 

The  points  at  which  the  clear  pulmonary  resonance  becomes  impaired 
should  be  marked  by  means  of  a  series  of  dots  with  a  skin  pencil  or 
ink.     Connecting  lines  between  these  dots  should  not  be  drawn  until 


Left  vagus 
nerve 


Right 


Right 

ventricle 


Left  auricle 


Fig.  170. — Vertical  anteroposterior  section  through  the  heart  showing  this  organ  from 
a  lateral  aspect.  In  following  the  curve  of  the  ribs  during  percussion  from  the  sternum  to 
the  axilla,  if  forcible  percussion  is  used  the  cardiac  dulness  obtained  will  be  equivalent  not 
only  to  the  lateral  boundary  of  the  organ  (which  we  wish  to  determine)  but  also  to  the 
depth  or  antero-posterior  diameter  (which  vitiates  the  results).  The  only  part  of  the  left 
auricle  which  approaches  the  anterior  chest  wall  is  its  appendage,  which  juts  around  the 
pulmonary  artery  and  if  greatly  enlarged  may  cause  an  increase  in  dulness  upward  and  to 
the  left.      (Compare  Fig.  163.) 


after  the  examination  is  complete,  lest  expectancy  warp  one's  judgment. 
The  right  border  requires  the  heavier  percussion;  the  heart  at  this  point 
recedes  from  the  chest  wall  and  its  location  is  often  determined  with 
difficulty.     Dulness  normally  extends  slightly  beyond  the  right  sternal 


PERCUSSION    OF    THE    HEART 


203 


border,  but  the  position  of  the  right-sided  dulness  varies  greatly  in  health. 
Very  light  percussion  should  be  used  for  the  left  border  and  especial  care 
should  be  exercised  to  deliver  the  percussion  blow  in  a  vertical  direction 
(see  Fig.  80). 

Unless  the  percussion  is  performed  with  great  care,  the  left  border  of 
the  heart  will  be  over-,  the  right  border,  under-estimated.  In  the  majority 
of  cases  percussion  of  the  cardiac  outline  by  a  skilful  examiner  yields 


Fig.  171. — The  deep  cardiac  dulness  corresponds  to  the  actual  size  of  the  heart.  In 
percussing,  we  generally  overestimate  the  extension  of  the  left  border  since  the  slope  of  the 
ribs  causes  the  percussion  stroke  to  fall  upon  the  side  of  the  heart  instead  of  solely  upon  its 
anterior  surface.  The  extension  of  the  right  border,  on  the  other  hand,  is  generally  under- 
estimated since  it  slopes  sharply  away  from  the  chest  wall  and  is  overlain  by  a  thick  section 
of  lung  tissue.  The  superficial  (absolute)  cardiac  dulness  represents  the  portion  of  the 
heart  which  is  uncovered  by  lung  tissue.  This  photograph  depicts  an  unusually  large 
superficial  dulness. 


results  which  are  sufficiently  accurate  for  most  clinical  purposes.  Such 
accuracy  consists,  however,  of  variations  in  centimeters,  not  millimeters. 
In  some  instances,  however,  other  methods  of  examination  such  as  ortho- 
diagraphy and  teleroentgenography  must  be  employed  and  in  all  in- 
stances percussion  should  be  controlled  by  palpation,  it  being  borne  in 


204  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

mind  that  the  left  border  usually  extends  1.5  cm.  beyond  the  lowermost 
and  outermost  point  at  which  the  heart  impulse  can  be  felt. 

The  portion  of  the  heart  which  is  uncovered  by  lung  yields  a  flat 
percussion  note.  This  area  is  known  as  the  superficial  cardiac  dulness. 
It  is  of  minor  importance  since  it  tells  us  more  concerning  the  state  of  the 
lungs  than  that  of  the  heart.  The  deep  cardiac  dulness,  on  the  other  hand, 
corresponds  to  the  size  of  the  heart.  It  may  be  determined  by  light  or 
moderately  heavy  percussion,  by  noting  the  points  at  which  clear  pul- 
monary resonance  ceases  and  slight  dulness  begins.  A  distinct  increase 
of  resistance  will  be  noted  at  similar  points.  Light  percussion  is  generally 
preferable  since  there  is  less  radiation  of  the  vibrations  and  a  keener 
perception  of  them  both  by  hearing  and  touch.1  The  superficial  area 
of  didness  is  absent  in  animals  and  in  some  people  with  long  thoraces  and 
freely  movable  hearts,  also  in  barrel-shaped  chests  with  large  lungs — 
emphysema.  It  is  enlarged  in  flat-chested  individuals,  in  tuberculosis — 
retracted  lungs — in  some  rachitic  deformities  and  in  pericardial  effusions. 
The  cardio-hepatic  angle  is  normally  acute,  with  its  concavity  toward  the 
right.  It  becomes  obtuse,  with  a  convexity  toward  the  right  in  pericar- 
dial effusions  and  in  right  ventricular  dilatation.  In  the  latter  condition 
an  interrupted  line — staircase  form — has  been  described. 

The  lower  cardiac  border  cannot  be  outlined  by  percussion  because  the 
heart  and  the  liver  overlap,  and  being  structures  of  relatively  equal 
densities  both  yield  a  similar  note.  Furthermore,  the  proximity  of 
Traube's  space  (Fig.  89)  adds  a  tympanitic  element  to  the  sound  and  as 
we  have  already  learned,  vibrations  cannot  be  localized  in  tympany 
producing  organs.  Orthodiagraphic  as  well  as  post-mortem  studies  have 
shown  that  the  heart  can  be  very  accurately  outlined  by  careful,  skilful 
percussion;  the  margin  of  error  should  in  the  average  case  not  exceed 
1  cm. 

THE  SIGNIFICANCE  OF  CARDIAC  DULNESS 

The  different  diameters  of  the  heart  bear  a  definite  relation  to  the 
age,  sex  and  height  of  the  individual.  Disproportionate  enlargement  of 
certain  diameters  is  quite  characteristic  of  certain  cardiac  lesions.  A 
satisfactory  method  of  recording  the  cardiac  dimensions  is  shown  in  Fig. 
173.  The  area  of  heart  dulness  is  normally  from  10  to  30  per  cent,  larger 
in  the  horizontal  than  in  the  erect  posture.  This  is  due  to  flattening  of  the 
chest  and  decreased  backward  convexity  of  the  dorsal  spine  in  the  former 
position.  In  the  erect  posture  the  heart  tends  to  fall  away  from  the  chest 
wall.  Furthermore,  the  heart  contains  more  blood  in  recumbency,  owing 
to  a  higher  venous  pressure;  its  systolic  output  is  larger. 

1  Moritz  found  that  with  light  percussion  for  the  right  and  threshold  percussion 
for  the  left,  cardiac  border,  the  former  corresponded  with  the  orthodiagraphic  findings 
in  86,  the  latter  in  70,  per  cent,  of  his  cases. 


Fig.  172. — -Heart  dulness  as  modified  by  disease.  These  figures  illustrate  the  more 
or  less  characteristic  shape  and  size  of  the  heart  as  a  result  of  different  cardiac  lesions. 
They  are  drawn  after  radiograms  and  correspond  to  the  areas  of  dulness  which  would 
be  obtained  by  skilful  percussion.     (After  F.  M.  Groedel.) 


PERCUSSION    OF    THE    HEART 


205 


Aortic  insufficiency. 


Aortic  obstruction. 


Mitral  obstruction. 


Mitral  insufficiency. 


Mitral  obstruction  and 
insufficiency. 


Aortic  obstruction  and 
mitral  insufficiency. 


Chronic  myocarditis. 
Fig.  172. 


206 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


Enlargement  toward  the  left  indicates  left,  sometimes  right,  ven- 
tricular enlargement.  An  increase  of  dulness  to  the  right  of  the  sternum 
may  be  due  to  right  auricular  dilatation  or  to  pericardial  effusion.  An 
enlarged  area  of  dulness  at  the  base  is  often  the  result  of  aortic  dilation  or 
aneurism.  The  left  auricle  being  a  posterior  chamber  cannot  be  outlined 
by  percussion.     Marked  enlargement  of  the  left  upper  cardiac  dulness 


Fig.   173. — Method  for  recording  cardiac  dulness. 


Fig.  174. — The  influence  of  respiration  upon  the  position  of  the  heart.    (Groedel.) 
Heavy  line:    normal   breathing.     Interrupted   line:   deep   expiration.      Dotted  line:   deep 

inspiration. 


may  result  from  dilatation  of  the  left  auricular  appendix  which  lies  just 
to  the  left  of  the  pulmonary  artery  (see  Fig.  163).  X-ray  studies  have 
shown  that  simple  mitral  insufficiency  never  causes  dilatation  of  the  left 
auricular  appendix,  but  in  mitral  stenosis  with  insufficiency  and  in  mitral 
insufficiency  during  broken  compensation  (tricuspid  insufficiency)  both 
dilatation  and  pulsation  are  demonstrable.1 

1  Pesci,  G. :  "L'augmento  di  volume  della  brecchietta  sinistra  del  cuore  nel  quadro 
radiologico."     Radiologia  med.,  I,  1914,  106. 


PERCUSSION    OF    THE    HEART 


207 


Increased  dulness  at  the  base  is  generally  due  to  dilatation  or  aneur- 
ism of  the  aorta  (Figs.  414,  417);  it  may  in  rare  instances  be  due  to  a 
patulous  ductus  arteriosus.  This  lesion  produces  a  quadrilateral  area  of 
dulness  to  the  left  in  the  second  (and  first)  interspace.  Accurate  outlining 
by  percussion  of  the  normal  aorta  and  pulmonary  artery  is  difficult  and 
erroneous  results  are  frequent,  owing  to  the  overlying  sternum. 

Method  of  Recording  the  Size  of  the  Heart. — After  outlining  the  heart 
by  percussion  and  drawing  lines  upon  the  skin  to  correspond  with  the 
area  of  dulness,  the  following  dimensions  should  be  measured  and  recorded. 

A  line  is  drawn  from  the  cardio-hepatic  angle  to  the  lowermost  portion 
of  the  left  border.     A  second  line  is  drawn  from  the  upper  border  of 


Fig.   175. — Moritz's  conjugates. 


cardiac  dulness  down  the  middle  of  the  sternum  to  connect  with  the  first 
line.  The  extremes  of  these  lines  are  connected  and  the  following  dimen- 
sions recorded  in  centimeters. 

Height  (S.  H.);  Left  oblique  (L.  S.);  Right  oblique  (R.  S.);  Right 
base  (R.  H.);  Left  base  (L.  H.)  (see  Fig.  173). 

These  dimensions  undergo  characteristic  variations  in  different  valvu- 
lar lesions,  owing  to  a  disproportionate  increase  in  the  size  of  different 
chambers.  Thus  the  left  base  is  increased  in  left  ventricular  hypertrophy 
and  in  mitral  insufficiency.  The  right  base  is  increased  in  tricuspid  lesions 
and  dilatation  of  the  right  auricle.  The  height  is  increased. in  aortic 
disease,  etc.  (Fig.  172). 

Moritz  has  suggested  a  somewhat  different  method  of  recording  the 
cardiac  area  which  has  found  considerable  favor,  the  dimensions  thus  ob- 
tained being  known  as  Moritz's  conjugates  (Fig.  175). 


208 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


It  has  been  shown  by  a  large  number  of  orthodiagraphic  studies  that 
the  normal  heart  bears  a  fairly  constant  relation  to  the  height  of  the  indi- 
vidual.    The  normal  averages  are  shown  in  the  following  table. 


Height  of  individual 


Men 


Women 


Cm. 


145-154 

155-164 
165-174 
175-187 


Feet  and 
inches 


MR 
Cm. 


ML 
Cm. 


L 
Cm. 


Cm. 


Cardiac 
area, 
Q  Cm. 


MR 

Cm. 


ML 
Cm. 


L 
Cm. 


Cm. 


4.7-5 
5 . 1—5 . 5 

5 . 5-5 . 9 
5.9-6.2 


3.5 

4.1 
4.2 
4.4 


7.9 

8.7 
8.8 
9.1 


12.5 
13.8 
14.1 
14.8 


9.7 

9.9 

10.3 

10.7 


95 
109 
116 
127 


3.5 
3.5 
3.8 


12.7 
13.2 
13.4 


Cardiac 

area, 

Q  Cm. 


9.4  93 

9 . 7       101 
9.9  !     105 


Fig.  176. — Pericardial  effusion.  Viewed  from  behind,  causing  enlargement  of  cardiac 
dulness  to  the  left  and  compression  of  the  left  lower  pulmonary  lobe.  The  left  ventricle  is 
hypertrophied,  the  mitral  valve  sclerotic.  The  liver  is  enlarged  and  upward  pressure  from 
ascitic  fluid  has  caused  compression  of  the  right  lower  lobe.  A,  aorta;  T,  trachea;  E, 
esophagus;  P. A.,  right  pulmonary  artery;  L.P.A.,  left  pulmonary  artery;  S.C.,  superior 
vena  cava;!/. A.,  left  auricular  appendage;  I.C.,  inferior  vena  cava.      (Compare  Fig.  216.) 

The  Orthodiagraph. — The  ordinary  X-ray  plate  is  inaccurate  for  the 
purpose  of  determining  the  size  of  the  heart.  The  reason  for  this  is 
the  fact  that  the  heart  lies  from  7  to  10  cm.  from  the  anterior  chest  wall. 


PERCUSSION    OF    THE    HEART 


209 


It  is,  therefore,  further  from  the  source  of  light  than  are  the  anterior  ribs 
and  since  the  X-rays  are  divergent  the  heart  shadow  varies  inconstantly 
and  disproportionately  in  relation  to  the  ribs. 

The  orthodiagraph  overcomes  this  difficulty  by  allowing  only  per- 
pendicular rays  to  fall  upon  a  fluorescent  screen  and  hence  a  parallel  pro- 


Fig.    177. — The  orthodiagraph.      {Hoffman.) 


jection  is  obtained.  The  patient  is  placed  between  the  source  of  light 
and  the  screen,  and  the  outline  cast  by  the  shadow  of  the  heart  in  its 
different  dimensions  is  plotted  upon  the  screen  from  which  it  can  be  ac- 
curately reproduced  and  measured. 

14 


CHAPTER  XIX 
AUSCULTATION 

In  ausculting  the  heart,  the  stethoscope  is  far  preferable  to  the  unaided 
ear  since  we  are  better  able  to  localize  sounds.  The  bell  of  the  stethoscope 
is  placed  especially  over  certain  areas  of  the  chest  wall  at  which  the  sounds 
produced  at  different  valvular  areas  are  best  heard.  These  areas  are 
named  after  the  valves  in  question.  It  is  to  be  remembered  that  these 
valvular  areas  do  not  correspond  to  the  anatomic  location  of  the  valves. 
Anatomically  the  valves  lie  very  close  together  (see  Fig.  125). 

The  heart  is  ausculted  to  determine  the  character  of  normal  sounds, 
the  presence  o£  abnormal  sounds,  and  the  regularity  of  cardiac  rhythm. 
When  the  heart  sounds  are  feeble  or  when  the  respiratory  sounds  are  un- 
duly loud,  it  may  be  necessary  to  have  the  patient  hold  his  breath  for 
brief  intervals  while  we  auscult.  The  procedure,  however,  if  long  con- 
tinued brings  about  abnormal  conditions  which  affect  the  heart,  and  in 
patients  suffering  from  marked  dyspnea  may  be  impossible.  In  deep- 
chested  individuals  it  is  often  advantageous  to  have  the  patient  lean 
forward  while  the  heart  is  being  ausculted,  a  procedure  which  brings  the 
heart  nearer  to  the  anterior  chest  wall. 

With  the  exception  of  the  pulmonary  valve,  the  sound  produced  at  a 
given  orifice  is  heard  best,  not  immediately  over  the  area  beneath  which 
the  valve  is  situated,  but  a  distance  from  it.  This  is  because  although 
the  sound  in  question  is  still -heard  over  its  specific  area,  the  other  sounds 
are  at  that  point  heard  less  distinctly. 

THE  ORIGIN  AND  CHARACTER  OF  THE  HEART  SOUNDS 

The  functional  activity  of  the  heart  produces  certain  sounds  which 
can  be  best  heard  over  the  precordium.  If  the  bell  of  the  stethoscope  is 
placed  over  the  left  lower  portion  of  the  precordium  (mitral  area)  two, 
occasionally  three,  distinct  sounds  will  be  heard.  The  sounds  are  in 
normal  cases  easily  differentiable  by  their  acoustic  qualities.  Under 
certain  abnormal  conditions  they  can  be  distinguished  only  by  timing 
their  occurrence  with  the  cardiac  impulse  or  if  this  is  invisible  and  impal- 
pable, by  palpating  the  carotid  pulse  which  occurs  0.1  second  after  ven- 
tricular systole.  The  two  sounds  mentioned  may  be  imitated  by  the 
syllables,  lubb-diipp. 

The  First  Sound. — The  first  sound  is  systolic  in  time  and  synchronous 
with  ventricular  contraction.  It  is  long,  more  or  less  loud,  low-pitched 
and  terminates  abruptly.  It  is  due  to:  (a)  muscular  contraction  of  the 
ventricles;  (6)  systolic  tension  of  the  auriculo-ventricular  valves;  (c) 
distention  of  the  aorta  and  pulmonary  artery.  It  is  loudest  over  the 
body  of  the  heart  but  also  heard  over  the  base.  It  is  normally  louder  as 
well  as  longer  (0.8  second)  than  the  second  sound  (0.05  second)  from 

210 


AUSCULTATION 


211 


which  it  is  separated  by  the  short  pause.  Systole  is  shorter  than  dias- 
tole, therefore  the  first  sound  is  preceded  by  the  long  pause. 

The  Second  Sound. — The  second  sound  marks  the  beginning  of  dias- 
tole, it  is  shorter,  less  loud,  higher-pitched  and  less  voluminous  than  the 
first  sound.  It  is  due  to  the  sudden  increase  in  tension  of  the  semilunar 
valves.  It  is  preceded  by  the  short  and  followed  by  the  long  pause.  It 
terminates  even  more  abruptly  than  the  first  sound. 

The  Third  Sound. — This  can  occasionally  be  heard  especially  in 
children,  in  the  left  lateral  decubitus,  and  if  the  heart  action  is  slow,  as 
a  faint  echo  of  the  second  sound.     It  occurs  early  in  diastole,  about  0.1 


Fig.  178. — Showing  the  areas  of  the  chest  over  which  sounds  produced  at  the  various 
valvular  orifices  are  generally  most  distinctly  heard.  A,  aortic  area;  P,  pulmonic  area; 
M,  mitral  area;  T,  tricuspid  area. 

The  unmarked  area  at  the  third  left  costo-sternal  articulation  is  one  at  which  aortic 
regurgitant  murmur  is  often  most  loudly  heard.  The  arrows  indicate  the  direction  of 
transmission  of  murmurs — the  obstructive  aortic,  into  the  carotids,  the  regurgitant  aortic, 
down  the  sternum  and  toward  the  apex;  the  regurgitant  mitral,  toward  the  axilla.  (Comp. 
Figs.  124  and  125.) 


second  after  the  second  sound,  and  when  sufficiently  marked,  causes  the 
protodiastolic  gallop  rhythm.  It  is  synchronous  with  the  early  normal 
diastolic  elevation  of  the  apex  cardiogram,  and  with  the  descending  limb 
of  the  "v"  wave  of  the  jugular  pulse.  When,  however,  allowance  is 
made  for  the  transmission,  the  impulse  of  the  protodiastolic  elevation  is 
found  to  be  synchronous  with  the  "h"  wave.  Thayer1  believes  the  third 
sound  to  be  due  to  the  sudden  tension  of  the  mitral  valve  which  occurs 
with  the  first  inrush  of  blood  at  the  beginning  of  diastole. 

The  rhythm  and  accentuation  of  each  sound  varies  with  the  location 


1  Thayer:  "Further  Observation  on  the  Third  Heart  Sound.' 
Amer.  Physicians,  May,  1909. 


Trims.    Assoc. 


212 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


at  which  it  is  heard.  At  the  mitral  area  the  first  sound  seems  louder — 
appears  to  bear  the  greater  stress.  Over  the  semilunar  valves  the  accent 
falls  upon  the  second  sound.  This  is  due  to  the  variation  in  distance 
between  the  point  of  origin  of  the  sound  and  the  location  of  the  stetho- 
scopic  bell. 


Aj>-proxima.te>  Musical  Eauivale?tt 


Electro -phonoaravh/ 


Fig.  179. — Diagrammatic  representation  of  the  heart  sounds,  and  the  pressure  curvea 
in  the  auricle,  ventricle  and  aorta.  D,  presphygmic  period;  E,  sphygmic  period;  F,  post- 
sphygmic  period. 

The  first  heart  sound  corresponds  to  a  vibratory  rate  of  about  55  per  second,  the  second 
sound,  to  a  rate  of  about  62.  The  latter  is,  therefore,  from  1  to  5  musical  notes  higher 
than  the  former.  Both  sounds  are  subject  to  considerable  individual  variation  both  as  to 
durationjand  pitch,  especially  the  second  heart  sound.  The  first  sound  begins  from  0.01 
to  0.02  seconds]  after  the  upstroke  of  the  apical  cardiogram,  and  ends  during  the  fall  of 
the  level  of  the  systolic  plateau,  generally  during  the  systolic  elevation  of  the  carotid 
pulse.      (Gerhartz.) 


THE  ACOUSTICS  OF  HEART  SOUNDS 

We  speak  of  a  heart  or  an  arterial  "tone"  or  sound  as  opposed  to  a 
murmur — a  distinction  made  by  Rouanet,  and  now  ineradically  custom 
sanctioned.  But  in  a  purely  physical  sense  such  a  differentiation  is 
entirely  unjustified  since  both  are  the  result  of  irregular  sonorous  vibra- 
tions. Indeed,  of  the  two,  the  vibrations  which  produce  a  "  murmur  "  are 
more  rhythmic  than  those  which  produce  a  "sound." 


AUSCULTATION  213 

Heart  sounds  are  produced  by  vibrations  of  the  muscular  or  mem- 
branous structures;  not  by  their  fluid  contents.  Sudden  increase  in 
valvular  or  arterial  tension  alone  may  produce  longitudinal  but  not  hori- 
zontal vibrations,  and  only  the  latter  are  capable  of  sound  production. 
If  an  elastic  band  which  has  been  stretched  is  plucked,  horizontal  vibra- 
tions are  set  up  and  a  sound  is  produced.  If  the  band  is  merely  suddenly 
stretched  by  pulling  upon  either  end,  longitudinal  vibrations  are  set  up 
but  unless  accidental  horizontal  vibrations  result  from  the  irregularity 
of  the  jerk  no  sound  results. 

A  membranous  sac  suddenly  distended  by  fluid  not  only  expands 
sufficiently  to  accommodate  the  increased  contents,  but  owing  to  its 
"inertia"  at  first  overexpands  and  in  turn,  owing  to  its  elasticity,  con- 
tracts. In  this  manner  a  series  of  transverse,  tone-producing  vibrations 
are  set  up.  Thus  arterial  sounds  are  produced  in  all  arteries  in  which 
the  disturbance  of  equilibrium  is  sufficiently  rapid.  Sclerotic  vessels 
are  less  distensible,  hence  the  arterial  sounds  over  such  arteries  often 
have  a  metallic  quality  owing  to  the  very  unrhythmic  vibrations  en- 
gendered by  the  stiffened  tissues.  Heart  sounds  arise  in  a  similar  man- 
ner. If,  owing  to  valvular  leakage  or  low  arterial  blood-pressure,  out- 
flow begins  before  a  rise  in  tension  sufficient  for  sonorous  vibration  occurs, 
the  sounds  are  weak  or  inaudible.  The  first  heart  "sound"  is  only  pos- 
sible, therefore,  if  a  presphygmic  period  of  increased  tension  precedes  the 
outflow  of  blood.  The  slower  the  pulse  rate,  and  the  lower  the  diastolic 
pressure,  the  easier  the  outflow  and  the  weaker  the  first  sound. 

The  First  Heart  Sound. — The  first  heart  sound  is  mainly  due  to  vibra- 
tions of  heart  walls  and  of  the  valves.  The  latter  elements  contribute  in 
no  small  measure  to  the  total  sound.  (The  intra-auricular  pressure  is  so 
low  compared  to  that  of  the  ventricles,  that  the  cuspid  valves  close  quickly, 
and  owing  to  their  anatomical  configuration  have  a  large  vibratory 
excursion.) 

Following  the  muscular  and  valvular  elements  of  the  first  sound  by 
0.06  to  0.07  second  (presphygmic  period)  the  vascular  element  due  to 
the  sudden  distention  of  the  aorta,  and  the  pulmonary  artery  occurs. 
Ordinarily  these  three  elements  are  fused  into  a  single  sound,  but  if  the 
presphygmic  period  is  delayed  the  different  sound  elements  become 
asynchronous  and  a  recognizable  splitting  of  the  first  sound  occurs. 

The  Second  Heart  Sound. — The  second  heart  sound  is  due  to  sudden 
increase  of  tension  and  subsequent  vibration  of  the  aortic  and  pulmonary 
valve  during  closure.  The  difference  in  intra-ventricular  and  intra-arterial 
pressure  at  the  end  of  systole  being  great,  especially  in  the  former  case, 
the  valves  snap  back,  and  vibrate  until  equilibrium  is  reestablished.  The 
sounds  produced  by  aortic  and  pulmonic  closure  while  not  quite  synchro- 
nous, are  separated  normally  by  too  short  a  time  interval  to  be  auditorily 
appreciable  as  separate  sounds.  When  pathologically  the  normal  pres- 
sure differences  are  exaggerated,  a  split,  second  sound  is  noted,  a  condition 
which  is  more  readily  appreciable  if  the  first  element  is  the  weaker  of  the 
two. 

Inasmuch  as  our  auditory  impressions  of  the  two  elements  of  the 
second  sound  are  always  to  some  extent  fused,  it  is  probable -that  we  can 
recognize  one  as  increased  over  the  other  only  when  at  least  a  2  to  1 
difference  in  intensity  prevails.  When  a  "marked  increase"  both  of 
pitch  and  intensity  of  the  pulmonic  second  sound  is  noted,  the  actual 


214  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

relative  intensity  is  several  times  greater.  In  attempting  to  estimate 
relative  differences  in  intensity  auscultation  should  be  practised  close 
to  the  sternal  margin  and  not  at  a  distance  from  it,  since  the  relative 
difference  tends  to  become  less  marked  in  the  process  of  conduction 
(Geigel). 


Fig.  180. — Section  of  the  thorax  viewed  from  in  front.  Systolic  (obstructive)  aortic 
murmurs  are  transmitted  in  the  direction  of  blood  flow,  upward  into  the  carotid  arteries. 
Systolic  (regurgitant)  mitral  murmurs  are  transmitted  in  the  opposite  direction  to  the 
blood  current,  toward  the  left  axilla,  being  conducted  thence  by  the  chordae  tendineae  and 
the  papillary  muscles.  A  =  aorta;  P=  pulmonary  artery;  C=  carotid  arteries;  P.M. 
=  papillary  muscle;  R  =  right  auricle;  iS  =  superior  vena  cava. 

THE  INDIVIDUAL  VARIATION  OF  HEART  SOUNDS 

There  is  no  absolutely  normal  standard  of  the  heart  sounds  and  a 
certain  allowance  must  be  made  for  individual  peculiarities.  As  a  gen- 
eral rule  such  variations  can  be  explained  either  upon  anatomic  grounds — 
the  size  of  the  lungs,  the  depth  of  the  chest,  etc.,  or  upon  the  basis  of  age 
and  sex. 


AUSCULTATION  215 

Substernal  Sounds. — In  a  considerable  number  of  perfectly  healthy 
individuals  the  heart  sounds  heard  just  above  the  ensiform  cartilage,  and 
in  its  immediate  vicinity,  have  a  peculiar  harsh,  scratching,  scraping  or 
crunching  quality  closely  resembling  a  pericardial  friction  sound.  This 
sound  which  has  been  described  as  the  xypo-sternal  crunch,  seems  super- 
ficial, is  increased  and  sometimes  audible  only  when  the  patient  leans 
forward  or  to  the  left.  It  is  short  and  heard  with  variable  intensity 
during  both  systole  and  diastole.  Its  etiology  is  uncertain.  Blumner 
has  suggested  that  it  is  due  to  changes  in  tension  of  the  loose  areolar 
tissue  in  the  sterno-pericardial  ligament.  This  sound  is  frequently  met 
in  cases  of  cardioptosis.  It  is  a  relatively  frequent  normal  phenomenon, 
the  importance  of  which  lies  in  the  fact  that  it  may  readily  be  mistaken 
for  a  pericardial  friction,  or  an  obstructive  mitral  murmur. 

The  Presystolic  Sound. — The  recent  electrophonographic  studies  of 
Bridgman  have  corroborated  by  means  of  graphic  records,  the  existence 
of  a  normal  presystolic  sound.  The  sound  in  question,  while  clinically 
unusual,  has  long  been  recognized  as  a  diagnostic  stumbling  block,  since 
it  may  closely  simulate  the  faint  presystolic  murmur  of  a  slight  degree 
of  mitral  stenosis. 

This  sound  is  perhaps  due  to  the  tension  of  the  ventricular  walls,  and 
the  fact  that  it  is  not  more  frequently  heard  appears  to  be  owing  to  the 
fact  that  the  sound  waves  are  normally  below  the  limits  of  human 
audibility. 

DISPROPORTIONATE    INTENSITY    OF    THE    HEART    SOUNDS 

The  relative  intensity  of  normal  heart  sounds  as  determined  with  the 
Oertel  stethoscope  by  Bock  are:  mitral  sound,  40;  pulmonic  sound,  18; 
aortic  sound,  20.  The  sound  heard  over  the  mitral  area  is  normally 
twice  as  loud  as  the  aortic. 

Accentuation  of  the  first  sound  is  due  to  increased  contractile  force  of 
the  papillary  and  ventricular  muscles.  It  occurs  after  exertion,  during 
overaction  (mental  excitement,  the  early  stages  of  fevers,  etc.)  and  in 
ventricular  hypertrophy. 

The  first  heart  sound  is  diminished  in  intensity,  assumes  the  quality  of 
the  second  sound,  in  protracted  fevers  (typhoid,  etc.),  in  some  valvular 
diseases,  especially  in  mitral  insufficiency,  and  in  fatty  infiltration  or 
degeneration  of  the  myocardium.  The  muscular  element  becomes  dimin- 
ished and  it  assumes  a  "valvular"  quality,  owing  to  the  preponderance  of 
its  second  sound  component,  i.e.,  the  snapping  back  of  the  mitral  valve. 

Accentuation  of  the  second  sound  indicates  increased  rapidity  of  closure, 
and  this  in  turn  relatively  increased  vascular  pressure,  in  the  aorta  or 
pulmonary  artery.  The  sound  is  due  not  to  the  mechanical  act  of  valvu- 
lar closure,  but  to  sudden  increase  in  tension  and  subsequent  vibration 
of  the  valves. 

The  pulmonic  second  sound  is  normally  louder  up  to  twenty-five  or 
thirty  years  of  age,  after  which  the  aortic  tends  to  become  louder.  'When 
auscultation  is  practised  (experimentally)  directly  over  the  vessels,  the 
aortic  sound  is  the  louder.  In  90  per  cent,  of  all  children  under  ten  years 
of  age,  the  pulmonic  sound  is  the  louder  (the  artery  is  more  superficial), 
and  in  about  10  per  cent,  of  the  cases  a  splitting  of  the  second  sound  can 
be  recognized. 


216  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

The  second  'pulmonic  sound  is  louder  in  the  recumbent  posture,  and  in 
conditions  which  increase  the  pressure  in  the  lesser  circulation — pulmo- 
nary consolidation,  pleural  effusion,  mitral  disease,  emphysema — provided 
the  right  heart  is  sufficiently  strong  to  maintain  the  increased  tension, 
i.e.,  the  tricuspid  valve  remains  competent.     When,  therefore,  we  say  that 


Fig.  181. — Left  ventricular  hypertrophy.  Extreme  hypertrophy  of  the  heart, 
especially  of  the  left  ventricle,  occurs  most  characteristically  in  aortic  valvular  disease,  or  as  a 
result  of  long-standing  arterial  hypertension.  It  is  clinically  characterized  by  1.  a  forcible, 
heaving  cardiac  impulse;  2.  displacement  of  the  apex  impulse  downward  and  to  the  left;  3.  a 
long,  low-pitched,  booming  first  sound;  and  4.  unless  the  aortic  valves  are  insufficient,  or 
myocardial  weakness  pronounced,  a  clear,  high-pitched,  ringing  accentuation  of  the  second 
sound  both  at  the  apex  and  at  the  aortic  area. 

the  second  sound  is  accentuated  we  mean  that  it  is  relatively  louder  than  it 
should  be  in  relation  to  age  and  posture.  This  phenomenon  indicates  in- 
creased pressure  in  the  lesser  circulation. 

The  aortic  second  sound  is  increased  in  arterial  hypertension,  provided 
the  ventricular  strength  be  sufficient.    This  occurs  especially  in  glomerulo- 


AUSCULTATION  217 

nephritis,  often  in  arterio-sclerosis  and  in  pregnancy  (increased  mass  of 
blood  or  blood-pressure) .  It  is  always  louder  than  the  pulmonic  sound  after 
the  sixth  decade.  Accentuation  of  the  aortic  second  sound  can  be  demon- 
strated in  about  two-thirds  of  the  cases  of  arterial  hypertension.  The  fact 
that  it  is  not  demonstrable  in  all  the  cases  may  be  due  to  the  presence  of 
obesity,  pulmonary  emphysema,  etc.  Occasionally  a  clear,  loud  metallic 
sound  is  heard  in  cases  of  syphilitic  aortitis  even  with  a  normal  blood- 
pressure,  showing  that  arterial  hypertension  is  not  the  only  determining 
factor.  The  aortic  second  sound  is  diminished  in  intensity  in  arterial 
hypotension  and  in  conditions  associated  with  imperfect  filling  of  the  aorta 
— mitral  or  aortic  obstruction,  exhausting  diarrhea,  and  when  the  semi- 
lunar valves  have  lost  their  elasticity. 

CHANGES  IN  THE  PITCH  OF  HEART  SOUNDS 

Increase  in  the  pitch  of  the  first  sound  occurs  when  contraction  is 
rapid;  increased  pitch  of  the  second  sound  occurs  when  the  semilunar 
valves  close  under  higher  tension.  When  marked,  the  latter  imparts  a 
ringing,  high-pitched,  metallic  quality  to  the  second  sound  which  is  quite 
as  indicative  of  increased  tension  as  is  the  actual  intensity  of  the  sound. 
When  air-containing  cavities  exist  near  the  heart  (pneumothorax,  pul- 
monary tuberculosis,  tympanitis,  etc.)  the  heart  sounds  may  also  take  on 
a  ringing,  metallic  quality  owing  to  the  resonating  properties  of  the  neigh- 
boring cavities. 

In  case  of  rapid  heart  action  and  low  blood-pressure — fevers,  muscular 
exertion,  etc.1 — the  first  sound  is  shorter,  more  snappy  and  higher  in 
pitch.  In  cardiac  hypertrophy  with  increased  blood-pressure  it  is  more 
booming  and  lower  in  pitch.  In  cardiac  dilatation  it  is  short,  sharp  and 
napping.  A  weak  first  sound  may  be  due  not  to  lack  of  force  but  to 
slowness  of  muscular  contraction.  The  quicker  the  contraction  and  the 
more  sudden  its  termination,  the  louder  the  sound  (Krehl).  In  children 
the  first  sound  is  more  snappy  and  high-pitched,  owing  to  a  preponder- 
ance of  the  valvular  sound  components. 

THE  REDUPLICATION  OF  HEART  SOUNDS 

Both  heart  sounds  are  composite.  If  any  one  of  the  component  ele- 
ments falls  out  of  time  a  reduplication  occurs,  two  sounds  instead  of  one 
being  heard.  If  the  time  interval  between  the  component  sound  elements 
is  a  short  one  we  speak  of  a  splitting  of  the  sound;  if  more  prolonged,  of 
a  reduplication.  The  introduction  of  some  abnormal  element  may  also 
cause  a  reduplication.  Instead  of  the  normal  lub-dupp  we  hear  tu-rub-b- 
lupp. 

Reduplication  of  the  first  sound  which  is  most  commonly  heard  at  the 
apex,  and  in  the  erect  posture,  is  probably  in  the  main  due  to  delayed 
contraction  of  the  papillary  muscles.  These  structures  being  supplied 
by  terminal  arteries,  are  readily  affected  by  fatigue  and  by  noxious  in- 
fluences. Reduplication  may,  however,  be  due  to  a  late  production  of 
the  vascular  element  (expulsion  tone),  especially  if  the  presphygmic 
period  is  prolonged.  It  is  often  heard  in  children,  in  thin-chested  indi- 
viduals, and  pathologically  in  arterio-sclerosis,  etc. 

Reduplication  of  the  second  sound  may  be  due  to :  (a)  abnormal  pressure 
relations  and  markedly  asynchronous  closure  of  the  aortic  and  pulmonic 


218 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


valves;  (b)  conditions  hastening  or  preventing  a  sudden  increase  in  ten- 
sion of  the  semilunar  leaflets — stiff  valves. 

Example. — A  deep  inspiration  increases  the  blood  in  the  lungs,  and 
decreases  the  amount  in  the  left  ventricle.  The  pressure  in  the  aorta, 
therefore,  increases  disproportionately  to  that  in  the  left  ventricle  and 
the  valves  close  more  quickly.  This  also  occurs  in  mitral  stenosis, 
whereas  the  condition  is  reversed  in  mitral  insufficiency.  Splitting  of 
the  first  sound  yields  an  anapestic  rhythm  (intervene)  w — .  Split- 
ting of  the  second  sound  yields  a  dactylic  rhythm  (merciful) — wo  (Cabot). 


Intriventr-icuUr 
TVe  ssi/re. 

Vent-rtcles 
rV-esijitoLtc  (Jillcp 


ra 


ii  a 


Split  setonl  souvi        j    [      Mj 


TrotoeLiistolic 

CfAllop 


7\ 


TC-LUB       DUB 


JT& 


I: 


kM 


ja 


Ml 


£3 


XI 


IUB      DUB      DA 


EI 


Fig.   182. — Illustrating  split  heart  sounds,  gallop  rhythms  and  their  phonetic  equivalent. 

(After  Hirschf elder.) 

Abnormal  accentuation  of  the  aortic  second  sound  indicates  increased 
arterial  pressure;  increased  intensity  and  pitch  of  the  pulmonic  second 
sound  points  to  increased  pressure  in  the  lesser  circulation. 


CHANGES  IN  THE  RHYTHM  OF  THE  HEART  SOUNDS 

When  from  any  cause  the  heart  is  weakened  and  the  diastolic  pause 
shortened,  the  heart  sounds  tend  to  become  equally  spaced  and  valvular 
in  character.  This  condition  is  known  as  "pendular  rhythm"  owing  to 
its  resemblance  to  a  ticking  clock.  It  is  generally  due  to  prolongation  of 
ventricular  systole,  and  hence  to  a  delay  in  the  appearance  of  the  second 
sound.  When  this  pendular  rhythm  is  associated  with  a  rapid  pulse  a 
disproportionate  shortening  of  diastole  occurs,  and  the  rhythm  is  spoken 
of  as  embryocardia  (fetal  rhythm) .  It  is  generally  associated  with  a  mono- 
crotic pulse  and  heard  in  cases  of  cardiac  dilatation. 

The  Presystolic  Gallop  Rhythm  (« — J)  "  symbolic." — In  this  condi- 
tion a  third  sound  is  introduced  into  the  cardiac  cycle  which  occurs  just 
before  ventricular  systole.  It  takes  its  name  from  its  similarity  to  the 
footfall  of  a  galloping  horse,  and  is  generally  due  to  abnormally  and 
audibly,  asynchronous  contraction  of  the  right  and  the  left  ventricles — ■ 
the  former  preceding.  It  is  sometimes  due  to  abnormally  loud  auricular 
contraction  and  hence  may  occur  when  these  chambers  are  hypertrophied 
as  in  the  early  stages  of  mitral  obstruction.  It  occurs  chiefly  in  cases  of 
arterial  hypertension  associated  with  a  dilating  hypertrophy.  Electro- 
cardiographically  it  is  almost  invariably  characterized  by  a  split  "R" 
wave.  Presystolic  gallop  rhythm  may  also  occur  in  the  course  of  acute 
infections,  especially  diphtheria,  scarlatina  and  rheumatic  fever.     It  is  a 


AUSCULTATION 


219 


distress  signal  from  the  heart  and  prognosis  is  worse  if  it  occurs  with 
hypo-  than  hypertension. 

The  Protodiastolic  Gallop  Rhythm  (w — )  "intervene." — This  is 
simply  an  exaggeration  of  the  normal  third  sound  and  is  due  to  the 
sudden  upward  snap  of  the  auriculo-ventricular  valves  early  in  diastole. 
It  is  generally  best  heard  at  the  base  of  the  heart.     It  occurs  especially 


Fig.  183. — Advanced  pulmonary  tuberculosis  of  the  left  lung  with  retraction,  consolida- 
tion, cavitation  and  cardiac  displacement  of  an  hypertrophied  heart  to  the  left.  In  such 
cases  the  heart  sounds  are  often  clearly  heard  over  the  whole  affected  side,  owing  to  di- 
minished reflection  at  the  heart-  (solid)  lung  junction  and  to  the  resonating  properties  of  the 
cavities.  Furthermore,  the  lung  is  generally  contracted  exposing  a  large  cardiac  surface  to 
the  chest  wall.  Still  another  factor  is  the  concomitant  emaciation  of  the  patient  resulting 
in  diminished  superficial  tissue.  Conduction  of  the  heart  sounds  to  the  opposite  side  of  the 
chest  in  right-sided  pulmonary  tuberculosis  was  pointed  out  by  J.  M.  DaCosta  and  is  some- 
times described  as  "DaCosta's  sign." 


when  the  rate  is  slow  and  corresponds  to  the  appearance  of  the  "h"  wave 
in  the  phlebogram.  It  is  heard  especially  in  mitral  obstruction,  aortic 
insufficiency,  and  adhesive  pericarditis. 

Occasionally  the  sound  may  be  heard  in  mid-diastole,  owing  to  the 
fact  that  the  auricles  begin  to  contract  at  this  time.  This  generally  indi- 
cates a  high  grade  of  cardiac  asthenia,  as  in  very  toxic  and"  prolonged 
cases  of  typhoid  fever. 


CHAPTER  XX 
HEART  MURMURS 

Acoustics. — Heart  murmurs  are  abnormal  sounds,  having  generally 
a  blowing  quality,  which  is  due  to  more  or  less  rhythmic  vibrations  of  the 
cardiac  or  arterial  tissues.  They  are  generally  produced  at  or  near  a 
valvular  orifice  by  abnormalities  in  contour  or  structure.  Such  condi- 
tions are  brought  about  (1)  either  by  organic  changes  which  result  in 
thickening,  stiffening,  roughening,  constriction,  dilatation,  perforation 
or  retraction  of  the  valvular  tissues  or  (2)  by  functional  lesions  resulting 
in  loss  of  muscular  tonus.  The  latter  occur  chiefly  at  the  mitral  and 
tricuspid  orifices.  Heart  murmurs  may  be  produced  (1)  when  blood  flows 
from  a  cavity  into  a  cylinder;  (2)  when  blood  flows  from  a  cylinder  into 
a  cavity;  (3)  when  membranes  vibrate  in  the  blood  stream;  (4)  when  the 
endocardium  or  intima  are  roughened. 

"Whatever  contracts  an  orifice,  whatever  dilates  a  cavity,  whatever 
establishes  an  orifice  or  a  cavity  where  none  should  be,  will  disturb  the 
even  flow  of  blood,  and  produce  vibration  and  a  murmur"  (Gee).  The 
heart  sound  consists  of  a  single,  intense,  demarked  auditory  impression. 
A  heart  murmur  gives  us  the  effect  of  unevenly  composed  sounds  which 
arise  from  rapidly  varying,  irregular,  sound  production.  The  heart 
sound  has  been  compared  to  a  single  stroke  upon  a  drum;  the  murmur,  to 
the  sound  produced  by  blowing  into  a  pipe.  The  sound  bears  the  same 
relation  to  the  murmur  as  does  a  pistol  shot,  to  the  surge  of  the  sea. 
The  difference,  therefore,  consists  in  the  suddenness  of  onset  and  of  ending 
of  the  sound,  as  compared  to  the  gradual  beginning  and  uncertain  termination 
of  the  murmur. 

The  fact  that  heart  murmurs  are  produced  by  vibrations  of  the 
tissues  and  not  by  the  vibrations  of  the  blood  stream  is  shown  by  the 
following  facts. 

I.  If  by  way  of  experiment  (Fig.  184)  we  introduce  a  flowing  stream  of 
water  by  means  of  a  tube  into  a  beaker  and  listen  with  a  stethoscope, 
(1)  above  the  fluid  level:  no  sound  is  heard.  (2)  If  the  bell  be  immersed, 
the  tube  mouth  being  at  "A" :  a  murmur  is  heard  at  "  C. "  (3)  If  the  tube 
be  raised :  the  murmur  becomes  feebler,  even  when  the  current  surrounds 
the  bell,  showing  that  the  sound  waves  are  not  produced  by  the  water 
directly,  but  by  the  vibrations  imparted  to  the  wall  of  the  beaker.  The 
sounds  increase  in  intensity,  the  nearer  the  tube  to  the  wall,  i.e.,  the  larger 
the  surface  contact  between  the  glass  and  the  fluid  vein.  On  withdrawal 
of  the  tube  all  sound  ceases,  despite  the  fact  that  the  current  still  per- 
sists for  a  time.  That  this  cessation  is  not  due  merely  to  an  inadequately 
rapid  current  is  shown  by  the  fact  that  pouring  H2S04  into  water,  which 
owing  to  greater  specific  gravity  and  the  generation  of  heat  must  cause 
much  more  rapid  currents,  does  not  alter  the  results. 

II.  Further,  it  can  be  shown  mathematically  that  the  sounds  pro- 
duced in  the  heart  and  blood-vessels  are  far  too  low  in  pitch  to  be  due 
to  sonorous  vibrations  produced  in  chambers  of  such  small  dimensions. 

220 


HEART    MURMURS 


221 


The  first  heart  sound  has  been  shown  by  Gerhardt  and  Funke,  to  corre- 
spond to  198  vibrations  per  second.  To  produce  by  fluid  vibrations  a 
sound  of  a  corresponding  pitch  to  that  of  the  heart,  would,  according  to 
Helmholtz's  formula  call  for  a  ventricle  with  a  capacity  of  about  24  liters! 
Although  these  figures  are  doubtless  high  owing  to  the  fact  that  Helm- 
holtz's formula  presupposes  a  cavity  communicating  with  the  atmosphere, 
yet  even  allowing  liberally  for  such  facts,  it  would  be  quite  impossible  to 
produce  sounds  similar  to  those  of  the  heart  or  of  murmurs  by  vibrations 
of  the  blood  columns  in  the  heart  and  great  vessels. 

Unquestionably  then,  heart  sounds  and  murmurs  must  be  due  to  horizontal  vibrations 
of  the  heart  and  vessel  walls  (Williams,  Kiwisch,  Weber).  The  heart  walls  and  the 
blood  stream  play  the  respective  parts  of  the  violin  string  and  the  bow  (Weber). 
The  mechanism  by  which  mural  vibrations  are  produced  is  as  follows: 
I.  In  flowing  from  "A"  to  "B"  (Fig.  185)  the  fluid  particles  deviate  from  their 
linear  course  and  produce  a  series  of  impactions  on  the  walls  of  "  B,"  because  the  adhe- 
sion between  the  wall  and  the  outer  fluid  layer  is  greater  than  the  cohesion  between 


^S\5 

A%& 


Fig.   185. 


Fig.  186. 


Fig.   187. 


Fig.  186a. 


the  fluid  particles.  This  tends  to  create  a  vacuum  at  "C"  which  in  turn  causes  the 
elastic  walls  of  "B"  to  fall  inward.  Such  a  movement  temporarily  overcomes  the 
vacuum,  thus  again  allowing  the  walls  to  regain  their  original  position.  A  regularly 
recurring  series  of  such  events  sets  up  continuous  lateral  vibrations  of  the  vascular 
walls  in  the  expanded  section  ("B").  In  the  constricted  portion  ("A")  a  series  of 
vibrations  is  established  by  alternate  suction  and  compression  engendered  in  "B. " 
These  vibratory  waves  have  "D"  as  their  nodal  point.  Rapidity  of  flow  greatly 
favors  murmur  production.  Clinically  the  production  of  murmurs  through  expan- 
sion of  the  blood  channels  finds  many  exemplifications — valvular  lesions,  aneurisms, 
etc. 

II.  The  reverse  condition,  in  which  there  is  a  sudden  contraction  of  the  blood 
channels,  may  also  produce  murmurs  (Fig.  186). 

Here  the  constriction  at  "  D  "  raises  the  pressure.  This  tends  to  force  the  stenotic 
opening  apart.  When  this  has  been  accomplished  pressure  temporarily  falls  again. 
Such  alterations  of  pressure  throw  the  vascular  walls  in  both  sections  "A"  and  "B" 
into  alternate  transverse  vibration.  The  ideal  conditions  for  the  production  of  a 
murmur  exist  in  case  of  fluid  flowing  through  a  constriction  (Fig.  I860). 

III.  Membranous  diaphragms,  e.g.,  heart  valves  or  vegetations  in  the  blood 
stream,  may,  by  flapping  like  a  sail  in  the  wind,  be  thrown  into  vibration,  and  may  be 
a  further  cause  in  the  production  of  murmurs  (Fig.  187).     (Compare  Fig.  212.) 


222  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

IV.  With  sufficient  rapidity  of  the  blood  current,  even  smooth-walled  vessels  of 
uniform  caliber  may  be  thrown  into  vibration  (this  has  been  demonstrated  by 
Weber),  for  no  vessel  is  absolutely  smooth;  and  slight  degrees  of  roughening  are  equiva- 
lent to  minute  stenoses.  Only  in  this  sense  can  murmurs  be  said  to  result  from 
"friction  of  the  blood  stream"  (Geigel).  "Fluid  of  any  kind,  flowing  at  any  speed 
through  a  cylindrical  tube,  will  not  cause  a  murmur,  even  if  the  tube  be  curved,  so 
long  as  it  retains  its  cylindrical  form"  (McLennan). 

THE  TECHNIQUE  OF  CARDIAC  AUSCULTATION 

I.  Place  the  bell  of  the  stethoscope  firmly  in  the  fourth  interspace  or 
over  the  fifth  rib  just  within  the  cardiac  impulse.  Ignore  the  respiratory 
sounds  and  determine  which  is  the  first  sound.  This  is  accomplished  by 
observing  (1)  that  it  is  synchronous  with  the  cardiac  impulse;  (2)  that  it 
follows  the  long  pause;  (3)  that  it  is  a  lower  pitch  as  well  as  longer  and 
louder  than  the  second  sound.  The  last  criterion  is,  of  course,  not  always 
reliable. 

Note  its  :  (1)  rate,  (2)  rhythm,  (3)  intensity,  (4)  quality,  (5)  duration, 
(6)  pitch  and  (7)  mode  of  beginning  and  of  termination. 

II.  Examine  the  sounds  heard  over  the  aortic,  pulmonic  and  tri- 
cuspid areas  in  a  similar  manner  (Fig.  187). 

VARIATIONS  IN  THE  INTENSITY  OF  HEART  SOUNDS 

Considerable  individual  variation  in  the  loudness  of  heart  sounds 
exists.     The  sounds  are: 

(a)  Decreased  in  recumbency,  in  adiposity,  in  men  with  great  mus- 
cular development,  in  women  with  large  mammae,  in  anasarca,  in 
pericardial  or  left-sided  pleural  effusions,  in  pulmonary  emphysema,  in 
myocardial  weakness  and  in  the  agonal  period.  Faint  irregular,  incoor- 
dinated  sounds  are  sometimes  heard  for  a  time  after  death  and  probably 
result  from  auricular  contractions,  since  the  right  auricle  is  the  last  part 
of  the  heart  to  die.  The  heart  sounds  may  be  very  faint  and  muffled 
even  in  perfect  health. 

(b)  Increased,  during  cardiac  overaction — physical  exertion,  mental 
excitement;  if  the  lungs  are  small,  or  if  they  are  retracted,  or  consolidated 
in  the  neighborhood  of  the  heart;  or  if  the  heart  is  hypertrophied. 

Occasionally  the  heart  sounds  can  be  heard  all  over  the  chest.  Changes 
in  the  relative  intensity  of  the  first  and  second  sounds  are  much  more  im- 
portant than  mere  changes  in  the  actual  intensity  of  both  sounds. 

Certain  facts  have  been  demonstrated  experimentally  which  have  prac- 
tical clinical  significance.  (1)  A  murmur  is  more  easily  produced,  if 
the  walls  of  the  tube  be  thin,  if  the  inner  surface  be  rough,  if  the  tube  be 
rigid,  and  if  viscosity  is  increased.  (2)  Increased  tension  has  very  little 
effect  provided  the  rate  remains  the  same.  (3)  Increasing  the  compres- 
sion of  the  tube  will  increase  the  murmur  up  to  a  maximum,  after  which 
it  tends  to  disappear.  (4)  With  a  certain  grade  of  rapidity  and  com- 
pression, the  murmur  becomes  finer  and  more  musical  (T.  Weber). 

From  the  standpoint  of  physics  no  sharp  distinction  can  be  drawn 
between  heart  sounds  and  murmurs  because  physically  speaking  both  are 
murmurs.  Heart  sounds  are  due  to  a  single  impulse  giving  rise  to  vibra- 
tions of  the  cardiac  or  vascular  wall;  a  murmur  is  due  to  repeated  vibra- 
tory impulses.  The  difference  is  similar  to  that  of  plucking  or  stroking 
a  violin  string.     Hence  sounds  are  generally  shorter  in  duration,  but  this 


HEART    MURMURS 


223 


is  not  an  essential  difference:  a  murmur  may  be  short  and  a  sound  long 
(for  example,  the  sound  of  a  kettle  drum  and  a  tuning  fork,  although 
each  is  produced  by  a  single  blow).  The  real  difference  lies  in  the  fact 
that  in  the  case  of  the  sound,  the  first  vibration  is  the  greatest,  whereas  in  the 
case  of  the  murmur,  we  have  at  the  outset  for  a  time,  a  continuous  series  of 
equal  vibratory  excursions. 

Impure  sounds  are  a  mixture  of  heart  sound  and  heart  murmur  with  no 
very  definite  preponderance  of  either.  Thus  in  a  given  case  one  observer 
would  say  "the  first  sound  is  murmurish,  impure,"  while  another  might 
with  equal  justice  and  correctness  say  there  is  "a  faint,  short  systolic 
murmur."  Impure  sounds  are  occasionally  heard  in  health,  but  indicate 
a  functionally  if  not  structurally  imperfect  valve  (roughness,  relaxation 
or  stiffness).  Under  exercise  they  often  develop  into  definite  murmurs. 
Sounds  are  to  a  certain  extent  conducted  along  the  arterial  wall,  but 
probably  not  to  any  great  degree  when  the  vessels  are  surrounded  by 
good  conducting  media.  There  is  also  some  conduction  by  the  fluid 
itself. 

ENDOCARDIAL  MURMURS 

Heart  murmurs  may  be  caused  by  perforation,  constriction,  dilatation, 
or  roughening  of  the  blood  channels,  especially  the  valvular  orifices. 
The  lesions  furnishing  these  conditions  may  be: 

1,  Organic. 

(a)  Obstruction  to  the  onward  flow  of  blood — stenosis. 

(b)  Valvular  insufficiency,  allowing  an  escape  of  blood  backward— 

regurgitation,  incompetency. 

2.  Functional  (without  structural  alterations)  insufficiency  of  the: 

(a)  Semilunar  valves — increased  arterial  pressure  and  dilatation  of  the 
aortic  or  pulmonic  rings. 

(b)  Cuspid  valves — relaxation  of  the  mitral  or  tricuspid  sphincters,  or 
improper  functionation  of  the  papillary  muscles. 

Relative  insufficiency  is  much  more  common  in  case  of  the  cuspid 
than  in  that  of  the  semilunar  valves.  Of  the  former,  the  tricuspid  is 
structurally  a  much  less  perfect  valve  than  is  the  mitral,  and  hence  is 
much  more  prone  to  leak  under  conditions  of  strain,  in  which  case  it 
acts  to  a  certain  extent  as  a  safety  valve  to  the  right  heart,  with  a  second 
line  of  defense  in  the  not  far  distant  liver,  against  which  the  blood  thrust 
of  the  right  heart  is  delivered. 

The  murmur  of  a  stenosis  is  produced  by  a  current  travelling  the 
normal  direction,  and  is  sometimes  spoken  of  as  an  onward  murmur.  It 
occurs  at  the  time  when  the  valve  should  be  open. 

The  murmur  of  an  insufficiency  is  produced  by  a  reflux  of  blood  and 
occurs  at  a  time  when  the  valve  should  be  closed — backward  murmur. 

The  Time  Relations  of  Valvular  Murmurs 


Systolic                                    Diastolic 

Insufficiency 

Obstruction 

Mitral 
Tricuspid 

Aorta 
Pulmonary  artery 

Aorta 
Pulmonary  arter-y 

(Presystolic) 
Mitral 
Tricuspid 

224  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

The  Differentiation  of  Valvular  Murmurs. — Several  murmurs  are 
often  coincidently  present  in  a  given  case  and  on  the  other  hand  the  same 
murmur  may  be  heard  over  different  areas  of  the  precordium.  In  such 
cases  we  judge  of  the  identity  or  non-identity  of  such  murmurs  by  the  follow- 
ing criteria:  (1)  location,  (2)  time,  (3)  transmission,  (-1)  quality,  (5) 
pitch,  (6)  duration,  (7)  intensity.  Among  these,  place,  time,  and  direc- 
tion of  conduction  are  by  far  the  most  important. 

The  Location  of  Murmurs. — A  murmur  is  generally  best  heard  at 
the  point  of  the  chest  wall  which  is  nearest  to  the  orifice  at  which  it  is 
produced.  The  location  at  which  the  different  valvular  sounds  are  best 
heard  has  already  been  considered  (p.  211).  The  same  rules  govern  the 
audibility  of  murmurs. 

The  Time  of  Murmurs. — It  is  essential  to  determine  the  exact  time 
and  duration  of  a  murmur  in  its  relation  to  the  cardiac  cycle — whether 
it  occurs  in  systole,  diastole  or  presystole.  This  is  accomplished  by 
noting  the  relation  of  the  murmur  to  the  (1)  apex  impulse,  (2)  first  sound, 
(3)  long  pause.  The  terms  protosystolic,  mesosystolic  and  telesystolic 
are  applied  to  murmurs  which  occupy  respectively  only  the  beginning, 
middle  or  end  of  systole. 

The  Transmission  of  Murmurs. — Murmurs  are  transmitted,  that  is 
they  are  heard  at  certain  areas  of  the  periphery  other  than  those  overlying 
the  location  of  their  origin,  or  of  their  normally  greatest  intensity. 
Murmurs  are  conducted  to  different  regions  generally  in  the  direction  of 
the  blood  current,  just  "as  wind  carries  sound."  Murmurs  are,  however, 
not  merely  conducted  to  the  surface  by  the  nearest  possible  route.  The 
sound-carrying  quality  of  the  neighboring  tissues  also  plays  a  most  im- 
portant role.  Thus  the  murmur  of  aortic  insufficiency  may  be  loudest 
over  the  ensiform  cartilage  whence  it  is  conducted  from  the  second 
right  interspace;  whereas  the  mitral  regurgitant  murmur,  produced 
deep  within  the  mediastinum,  is  conducted  in  an  opposite  direction  to 
that  of  the  blood  flow,  by  means  of  the  papillary  muscles,  to  the  region  of 
the  cardiac  apex,  the  axilla,  or  the  scapular  angle. 

The  Quality  of  Murmurs. — Murmurs  vary  in  quality  and  are  hence 
described  as  being  musical,  non-musical;  harsh,  soft;  blowing,  scraping; 
squeaking,  etc.  The  pitch  is  also  of  great  importance.  These  facts  are 
significant  since  they  aid  one  in  distinguishing  between  murmurs  when 
two  or  more  are  present.  It  is  to  be  remembered,  however,  that  a  mur- 
mur may  undergo  modification  dependent  upon  the  point  at  which  one 
auscults ;  and  further,  that  the  same  murmur  may  change  very  considera- 
bly in  quality  as  a  result  of  numerous  conditions  such  as  myocardial 
weakness,  exercise,  posture,  blood-pressure,  etc.  One  cannot  judge  of 
the  type  or  seriousness  of  a  lesion  by  the  quality  or  intensity  of  the  mur- 
mur. Indeed,  a  loud  murmur  may  denote  a  good  heart  muscle  and  a 
weak  murmur,  myocardial  weakness.  When  the  latter  is  marked  an 
organic  murmur  previously  present  may  disappear  entirely  to  reappear 
when  compensation  improves.  As  a  general  rule,  however,  musical  and 
scratchy  endocardial  murmurs  are  rarely  functional.  When  an  organic 
lesion  is  progressive,  the  murmur  increases  in  intensity  up  to  a  certain 
point,  beyond  which  it  recedes,  either  as  the  result  of  muscular  weakness 
or  on  account  of  the  extent  of  the  valvular  damage.  Systolic  murmurs 
are  generally  louder  than  diastolic  murmurs,  especially  in  recumbency. 
On  account  of   their  faintness  and  low  pitch,   diastolic  murmurs  are 


HEART    MURMURS 


225 


easily  overlooked.  Systolic  murmurs  may  be  present  when  the  patient 
lies  down  and  may  disappear  when  he  is  erect.  Obstructive  murmurs 
are  generally  louder  in  the  erect  posture.  Aortic  and  pulmonic  murmurs 
are  less  affected  by  posture  than  those  produced  at  the  mitral  or  tricuspid 
orifices.  Most  murmurs  are  louder  after  exertion,  and  some  may  require 
physical  exercise  to  make  them  audible.  Hemic  murmurs  resulting 
either  from  anemia  alone,  or  from  anemia  together  with  a  dilatation  of 


a  v 


Fig.   188. — Diagram  illustrating  heart  sounds  and  murmurs. 

A:  Normal  heart  sounds.  A,  auricular  sys'tole;  V,  ventricular  systole;  D,  ventricular 
diastole.      The  sounds  begin  and  end  abruptly. 

B:  Systolic  murmur  following  first  sound.      The  first  sound  terminates  gradually. 

C:  Systolic  murmur  accompanying  first  sound.  The  first  sound  is  "impure"  and  fades 
away  gradually. 

D:  Systolic  murmur  replacing  first  sound.  The  first  sound  is  supplanted  by  a  blowing 
sound. 

E:  Diastolic  murmur  following  the  second  sound.  The  second  sound  is  followed  by  a 
blowing  sound. 

F:  Diastolic  murmur  accompanying  the  second  sound.  The  second  sound  fades  away 
gradually. 

G:  Diastolic  murmur  replacing  the  second  sound.  Instead  of  a  clear-cut  second  sound 
one  hears  a  blowing  sound.  This  is  often  low  pitched  and  heard  with  difficulty.  The  ab- 
sence of  the  second  sound  always  suggests  careful  investigation. 

H:  Late  diastolic  murmur. 

I:  Continuous  systolic  and  diastolic  murmur  in  patent  ductus  arteriosus. 


the  pulmonary  artery,  are  best  heard  at  the  pulmonic  area.  They  are 
soft  and  blowing,  low  in  pitch,  variable  in  character,  indefinite  in  trans- 
mission. Murmurs  are  also  described  as  being  crescendo  or  diminuendo 
in  character,  the  terms  being  used  in  the  musical  sense  tcr  indicate  a 
continuous  increase  or  decrease  respectively  of  their  intensity.  The 
murmur  of  mitral  stenosis  is  often  typically  crescendo,  that  of  aortic 
insufficiency  often  diminuendo,  in  quality. 

15 


226  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

Even  organic  murmurs  may  be  variable  in  quality  .and  intensity 
to  the  point  of  actual  disappearance,  either  constantly  or  intermittently 
in  a  series  of  successive  cardiac  cycles.  Such  variation  is  not  uncommon 
in  auricular  fibrillation,  extrasystole  and  heart  block  owing  to  variable 
degrees  of  auriculo-ventricular  coordination  and  rate  of  blood  flow.  With 
the  onset  of  auricular  fibrillation  or  of  paroxysmal  tachycardia,  murmurs 
often  disappear  entirely,  to  return  when  the  normal  rhythm  is 
reestablished. 


Fig.  189. — Aortic  obstruction.  The  aortic  leaflets  are  fused  together  as  the  result  of 
inflammatory  adhesion,  leaving  only  a  small  elliptical  opening.  The  arrow  indicates  the 
direction  of  blood  flow.  The  physical  signs  of  aortic  obstruction  are  a  systolic  thrill  and  a 
loud  crescendo  murmur  at  the  base  of  the  heart,  the  latter  being  transmitted  into  the 
carotid  arteries.  The  pulse  is  small  in  volume  and  the  systolic  plateau  shows  a  long,  slow, 
gradual  ascent  and  descent. 

The  left  ventricle  becomes  greatly  hypertrophied  and  hence  the  cardiac  impulse  is  dis- 
placed downward  and  outward,  and  the  longitudinal  diameter  of  the  heart  is  increased. 
When  as  is  usually  the  case,  mitral  insufficiency  exists,  the  vertical  diameter  is  also  in- 
creased.    (See  Fig.  172.) 

INDIVIDUAL  VALVULAR  MURMURS 

1.  The  systolic  aortic  murmur  results  from  roughening  or  obstruction 
at  the  aortic  orifice,  or  dilatation  of  the  aorta.  It  is  best  heard  at  the 
second  or  third  left  intercostal  space  and  is  transmitted  into  the  carotid 
arteries.     Phonetic  equivalent:  Lu-f-f-f-Dupp. 

2.  The  diastolic  aortic  murmur  results  from  insufficiency,  retraction, 
separation  (vegetations)  or  perforation  of  the  aortic  leaflets.  It  is  best 
heard  at  second  right  or  fourth  left  intercostal  space,  close  to  the  sternum, 
and  is  transmitted  toward  the  apex  and  to  the  ensiform  cartilage.  Pho- 
netic equivalent:  Lub  Duf-f-f  (Fig.  417). 


HEART    MURMURS 


227 


Fig.  190. — Aortic  roughening  and  calcification.  The  aortic  valves  are  stiffened  and 
calcareous,  the  mouths  of  the  coronary  arteries  are  involved  in  the  arterio-sclerotic  process. 
The  left  ventricles  and  papillary  muscles  are  hypertrophied. 

Physical  signs.  A  systolic  aortic  murmur  transmitted  into  the  carotid  arteries.  A 
forcible  heaving,  cardiac  impulse  displaced  downward  and  to  the  left.  A  loud  booming  first 
sound;  a  clear-cut,  ringing,  high-pitched,  accentuated  aortic  second  sound.  This  lesion  is 
very  common  in  advanced  years  and  is  often  erroneously  diagnosticated  as  aortic  obstruction. 


Fig.  191. — Aortic  obstruction.  The  dotted  areas  indicate  the  locations  over  which  the 
systolic  aortic  murmur  may  be  heard.  On  the  precordium  has  been  drawn  a  diagram  to 
illustrate  the  relationship  of  the  murmur  to  the  heart  sounds. 


228 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


3.  The  systolic  mitral  murmur  is  due  to  valvular  insufficiency,  which 
may  result  from  retraction,  perforation  or  vegetations  upon  the  valvular 
curtains;  also  from  shortening  of  the  chordae  tendinese;  or  from  dilatation 
of  the  mitral  sphincter.  It  is  best  heard  at  the  mitral  area  and  is  con- 
ducted toward  the  left  axilla  and  sometimes  to  the  angle  of  the  left- 
scapula.  The  former  is  in  reverse  of  the  direction  of  the  blood  stream, 
and  is  mainly  due  to  conduction  b}^  means  of  the  papillary  muscles. 


Fig.  192. — Aortic  aneurism.  Showing  a  heart  with  the  left  ventricle  exposed,  the 
aortic  valves,  and  beyond  them  a  large  aortic  aneurism.  Such  a  sudden  widening  of  the 
blood  channel  (aorta)  sets  up  eddies  in  the  blood  stream  and  will  cause  a  systolic  murmur  if 
the  current  is  sufficiently  rapid  and  if  the  aneurism  is  not  filled  with  a  blood  clot.  In  many 
cases  of  aneurism  the  aortic  valves  are  incompetent,  owing  to  dilatation  of  the  aortic  lumen 
and  thus  a  diastolic  (regurgitant)  murmur  is  superadded.  The  double  and  more  or  less 
continuous  murmur  with  a  rhythmic  accentuation  due  to  systole  is  known  as  a  bruit. 

"The  chordae  tendinese  transmit  the  mitral  murmur  from  the  mitral  seg- 
ments to  those  portions  of  the  heart  into  which  they  are  inserted."1  The 
murmur  heard  in  the  left  axilla  in  mitral  insufficiency  is  chiefly  due  to 
the  proximity  of  the  insertion  of  the  anterior  papillary  muscle  and  de- 
pends only  in  small  part  upon  conduction  by  means  of  the  ventricular 

xDe  Satjtelle  and  Grey:  Arch.  Int.  Med.,  December,  1911. 


HEART    MURMURS  229 

wall.  The  experimental  transplantation  of  a  papillary  muscle  alters  the 
direction  of  murmur  transmission.  The  posterior  papillary  muscle  often 
conducts  the  mitral  regurgitant  murmur  to  the  scapular  angle.  At  times 
the  murmur  produced  at  an  incompetent  mitral  orifice  is  heard  over  the 
dilated  left  auricular  appendage — in  the  third  left  intercostal  space. 
Phonetic  equivalent:  Luf-f-f  Dupp. 

4.  The  presystolic  mitral  murmur  is  the  result  of  mitral  obstruction. 
It  is  heard  best  at  or  just  within  the  apex.     Often  one  of  its  chief  char- 


Fig.  193. — Cardiac  hypertrophy.  The  cor  bovinum  occurs  characteristically  in  aortic 
disease.  It  is  clinically  manifested  by:  displacement  of  the  cardiac  impulse,  downward  and 
to  the  left;  a  forcible  heaving  impulse,  and  a  loud,  low-pitched  booming  first  sound.  It 
generally  results  from  aortic  insufficiency  beginning  in  early  life. 

acteristics  is  its  crescendo  quality,  which  has  been  ascribed  to  (a)  powerful 
diastolic  ventricular  suction,  (6)  to  auricular  systole,  (c)  to  increased 
pressure  in  the  pulmonary  circulation.  It  is  often  associated  with  a 
snappy,  high-pitched  first  sound.  It  is  rough  and  rumbling  in  character, 
and  often  followed  by  a  systolic  murmur — -because  a  valve- which  is  suffi- 
ciently indurated  to  produce  an  obstruction  is  generally  incapable  of 
complete  systolic  closure  (insufficiency).  It  is  generally  accompanied 
by  a  fine  presystolic  thrill,  and  if  the  right  heart  is  competent  by  an 


230 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


accentuated  pulmonic  second  sound.  The  murmur  is  most  intense  when 
blood  flow  is  most  rapid — when  the  differential  pressure  between  auricle 
and  ventricle  is  greatest.  Hence,  the  murmur  of  mitral  obstruction  may 
occupy  any  part  of  the  diastolic  interval.  Thus  with  a  slowly  beating 
heart  and  a  powerful  auricle  the  murmur  appears  in  presystole.     If,  how- 


Fig.  194. — Aortic  and  mitral  insufficiency  due  to  acute  endocarditis.  Fresh 
vegetations  are  seen  on  the  respective  valves.  The  heart  is  hypertrophied,  the  aorta  normal. 
The  arrows  indicate  the  direction  of  the  regurgitant  blood  stream.  The  murmur  is  trans- 
mitted from  the  aortic  valves  downward  toward  the  apex,  in  the  direction  of  the  blood 
flow.  In  the  case  of  the  mitral  valve  it  is  conducted  in  a  reverse  direction  to  that  of  blood 
flow,  toward  the  axilla  and  the  angle  of  the  scapula,  by  means  of  the  papillary  muscles. 
A,  anterior  and  P,  posterior,  papillary  muscle.     L.A.A.,  left  auricular  appendix. 

Physical  signs.  A  heaving  impulse,  displaced  downward  and  to  the  left,  pulsating  caro- 
tid arteries,  a  water-hammer  pulse.  Cardiac  dulness  enlarged  to  the  left.  A  diastolic  aortic 
murmur  transmitted  to  the  ensiform  cartilage;  a  systolic  murmur  conducted  to  the  axilla 
and  the  scapular  angle.      (Compare  Figs.  172,  181.) 


ever,  stenosis  is  marked  and  the  pulse  rate  rapid,  "an  early  diastolic 
rumble  may  be  added;  the  period  of  silence  between  the  two  murmurs 
corresponds  to  the  period  when  filling  is  at  its  slowest"  (Lewis).  The 
intensity  of  the  murmur  is  in  most  instances  increased  by  exercise  or  the 
recumbent  posture,  which  factors  increase  the  cardiac  output. 

In  addition  to  the  rumbling  presystolic  murmur  heard  near  the  cardiac 


HEART    MURMURS 


231 


apex  in  mitral  obstruction,  a  soft,  blowing,  early  diastolic  murmur  is 
often  heard  along  the  left  sternal  margin.  This  murmur  is  due  to  dilata- 
tion of  the  pulmonary  artery  which,  if  sufficiently  marked,  causes  an  in- 
sufficiency of  the  pulmonary  leaflets. 


Fig.  195. — Diagram  illustrating  the  direction  of  the  regurgitant  blood  stream  in  aortic 
insufficiency.  The  murmur  is  best  heard  at  the  second  right  costo-sternal  articulation  and 
is  transmitted  toward  the  ensiform  cartilage  and  toward  the  cardiac  apex. 


Fig.  196. — Aoktic  insufficiency.  The  dotted  areas  indicate  the  locations  over  which 
the  diastolic  murmur  may  be  heard.  The  circle  contains  a  diagrammatic  representation 
of  the  murmur  in  relation  to  the  first  and  second  heart  sounds 


Thus  mitral  stenosis  complicated  by  relative  pulmonary  insufficiency 
may  closely  simulate  aortic  insufficiency  with  a  Flint  murmur.  But  in 
the  latter  case  left  ventricular  hypertrophy  is  greater,  the  blood-pressure 
picture  is  quite  characteristic,  and  other  pulsatory  phenomena  such  as  a 
capillary  pulse,  Duroziez's  murmur,  etc.,  will  establish  the  diagnosis. 

The  difficulty  so  many  students  have  in  recognizing  or  even  being 
able  to  identify  presystolic  murmurs  is  due  to  the  fact  that  they  expect 


232  THE    EXAMINATION    OF    CIRCULATOBY    SYSTEM 

to  hear  a  swishing  sound  similar  to  that  produced  by  systolic  or  diastolic 
murmurs.  The  presystolic  murmur  is  a  sound  very  different  in  quality. 
It  is  a  rumble  somewhat  like  a  short  roll  on  the  drum,  which  precedes  and 
gradually  merges  into  the  first  sound  of  the  heart. 

When  the  heart  becomes  dilated  and  the  auricle  paralyzed,  the  mur- 
mur disappears,  and  fibrillation  of  the  auricle  makes  its  appearance.  The 
crescendo  quality  while  clinically  characteristic  has  been  shown  to  be  due, 
not  to  an  inherent  quality  of  the  murmur  but  chiefly  to  the  proximity  of 


Fig.  197. — Mitral  insufficiency.  The  mitral  curtains  are  thickened,  and  are  the  seat 
of  numerous  vegetations.  Some  of  the  chordse  tendinese  are  ruptured,  all  of  them  are 
thickened  and  shortened.  The  left  ventricle  is  hypertrophied.  The  murmur  of  mitral 
insufficiency  is  systolic  in  time.  It  is  transmitted  toward  the  left  axilla  and  scapula  in 
reverse  of  the  direction  of  the  blood  stream  by  the  papillary  muscles  and  the  chorda;  ten- 
dinese.    The  arrow  indicates  the  direction  of  the  regurgitant  blood  stream. 

the  first  heart  sound.  If  the  auricle  goes  into  a  state  of  fibrillation  or  if 
it  loses  its  contractile  force  because  of  extreme  dilatation,  the  presystolic 
murmur  disappears  and  instead  of  it  a  murmur  is  heard  early  in  diastole. 
Pure  presystolic  murmurs  can  arise  only  at  the  auriculo-ventricular  ori- 
fices. Phonetic  equivalent:  R-R-R-upp,  Dupp  (presystolic  rumble); 
Rup-Tut-Rarou  (mid-diastolic  rumble)  (see  Fig.  202). 

5.  The  systolic  tricuspid  murmur  is  heard  at  the  tricuspid  area,  be- 
cause both  the  right  auricle  and  ventricle  lie  immediately  beneath  this 
point.     It  is  also  often  heard  over  the  mitral  area,  and  cannot  always  be 


HEART    MURMURS  233 

differentiated  from  the  murmur  of  a  mitral  insufficiency,  with  which  it 
is  usually  associated.  The  presence  of  marked  right  heart  dilatation, 
of  a  positive  venous  pulse,  of  an  enlarged  or  even  pulsating  liver,  pulmo- 
nary congestion,   ascites,   etc.,   enable  us  to  definitely   state   that   the 


Fig.  198. — Mitral  insufficiency.  The  left  ventricle  is  hypertrophied,  the  left  auricle 
dilated.  The  direction  of  the  regurgitant  blood  flow,  as  indicated  by  the  arrow,  is  upward 
and  backward,  but  the  murmur  is  transmitted  chiefly  downward  and  forward  through  the 
vibrating  chorda?  tendinea?  and  the  papillary  muscles.  A,  aorta;  L.A.,  left  auricle;  Ft. A., 
part  of  right  auricle;  P,  portal  vein;  R.P.,  right  pulmonary  artery;  L.P.,  left  pulmonary 
artery;  T,  trachea;  S.A.,  right  subclavian  artery;  S.V.,  right  subclavian  vein. 

tricuspid  valve  is  incompetent.  A  diagnosis  of  tricuspid  "insufficiency, 
based  merely  upon  the  fact  that  a  systolic  murmur  is  clearly  audible  at 
the  tricuspid  area  is  not  justified.  Such  a  diagnosis  may  on  the  con- 
trary be  eminently  warranted  in  the  absence  of  a  tricuspid  murmurif 


234 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


the  presence  of  a  positive  venous  pulse  or  a  pulsating  liver  can  be 
demonstrated.     Phonetic  equivalent:  Luf-f-f  Dup  (see  Figs.  211,  381). 

6.  The  presystolic  tricuspid  murmur  is  heard  at  the  tricuspid  area  and 
results  from  obstruction  of  that  orifice  (see  Fig.  202).  This,  as  an  isolated 
lesion,  is  very  rare.     It  is  usually  associated  with  mitral  obstruction  and  is 


Fig.  199. 


Fig.  200. 

Figs.  199  and  200. — Mitral  insufficiency.  The  dots  indicate  the  area  over  which  the 
systolic  mitral  murmur  is  generally  audible.  The  small  circle  indicates  the  accentuated 
pulmonic  second  sound  (pulmonary  arterial  hypertension).  The  large  circle  contains  a 
diagrammatic  representation  of  the  relation  of  the  murmur  to  the  heart  sounds.  When  loud 
it  is  often  audible  at  the  angle  of  the  left  scapula. 

of  "rheumatic"  origin.  A  large  "a"  wave  in  the  liver  pulse  is  said  to  be 
suggestive  of  the  condition.  A  few  cases  have  been  diagnosticated  during 
life;  most  of  the  cases  found  at  autopsy  go  to  the  table  with  a  diagnosis 
of  "mitral  obstruction." 

7.  The  systolic  pulmonic  murmur  if  organic  in  nature  is  generally  due 
to  a  congenital  deformity  of  this  orifice  which  results  in  obstruction.     It 


HEART   MURMURS  235 

is  loud  and  best  heard  at  the  pulmonic  area  and  may  be  transmitted  to 
the  subclavicular  region  (along  the  pulmonary  arteries).  It  is  associated 
with  marked  cyanosis,  clubbing  of  the  fingers,  dyspnea  and  if  the  child 
lives  long  enough,  often  with  pulmonary  tuberculosis.  It  is  accompanied 
by  a  systolic  thrill  at  the  base  of  the  heart,  a  weak  pulmonic  second  sound, 
and  hypertrophy  of  the  right  heart.  Phonetic  equivalent:  Luf-f-f  Dup 
(see  Figs.  1,  209,  310). 

Many  functional  murmurs  arise  at  the  pulmonary  orifice,  and  most 
pulmonic  murmurs  are  functional.  Experimentally,  when  the  heart  is 
exposed,  the  slightest  compression  or  traction  upon  the  artery  is  sufficient 


Fig.  201. — Mitral  obstruction.  Showing  the  area  over  which  the  diastolic  (presys- 
tolic) mitral  murmur  is  generally  audible,  together  with  a  diagrammatic  illustration  of  its 
relation  to  the  heart  sounds.  Accentuation,  splitting  or  reduplication  of  the  pulmonic 
second  sound  is  an  invariable  accompaniment  of  this  lesion  until  compensation  fails. 

to  produce  a  murmur.  Such  pressure  may  easily  be  produced  in  health 
by  change  of  posture,  forced  held  inspiration,  slight  pleural  adhesions, 
etc.  The  pulmonary  area  was  named  by  Balfour  the  " region  of  romance" 
because  so  many,  variable,  inconsequential  murmurs  may  be  heard  in 
this  region.  There  are,  however,  some  cases  of  mitral  insufficiency  in 
which  the  regurgitant  murmur  is  heard  near  the  second  left  intercostal 
space,  owing  to  the  proximity  of  the  left  auricular  appendage  (Figs. 
163,  170). 

A  diagnosis  of  pulmonary  stenosis  based  solely  upon  the  presence  of  a 
systolic  murmur  at  the  second  left  intercostal  space  is  absolutely  un- 
justified. Pulmonary  stenosis  is  a  rare  and  nearly  always,  congenital 
lesion  which  is  associated  with  cyanosis,  clubbed  fingers,  cardiac  hyper- 
trophy and  a  feeble  second  sound. 

8.  The  diastolic  pulmonic  murmur  (pulmonary  insufficiency)  may 
result  from  congenital  disease,  or  from  ulcerative  endocarditis;  in  either 


236  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

case  it  is  a  rare  lesion.  It  may  be  due  to  functional  dilatation  of  the  pul- 
monary orifice  under  severe  strain  which  leads.to  increased  blood-pressure 
in  the  lesser  circulation.  It  is  best  heard  over  the  second  right  intercostal 
space,  seems  superficial,  is  loud,  not  infrequently  musical  and  may  be 
associated  with  a  markedly  accentuated  pulmonic  second  sound.  The 
right  ventricle  is  hypertrophied.  It  is  differentiated  from  the  aortic  re- 
gurgitant murmur  by  the  fact  that  it  is  not  transmitted  to  theensiform 
cartilage  nor  toward  the  apex,  and  that  it  is  unassociated  with  a'Corrigan 
pulse,  and  with  the  blood-pressure  picture  so  characteristic  of  the  latter 
lesion.     Phonetic  equivalent:  Lub-Duf-f-f. 


Fig.  202. — Aortic,  mitral  and  tricuspid  obstruction.  The  lesions  depicted  are  the 
end  result  of  acute,  generally  rheumatic,  endocarditis.  The  mitral  orifice  shows  a  typical  but- 
tonhole deformity  with  induration  and  calcification.  The  tricuspid  orifice  shows  a  uniform 
constriction,  while  the  aortic  leaflets  are  fused  together  and  sclerotic,  with  secondary  cal- 
careous infiltration.  Tricuspid  stenosis  as  an  isolated  lesion  is  rare.  It  may  be  due  to  the 
same  etiologic  factors  as  the  mitral  lesion  (generally  rheumatic  fever)  or  may  be  the  result 
of  the  mitral  lesion,  which  by  overstraining  the  right  ventricle  leads  to  edema,  hemorrhage 
and  subsequent  fibrosis  of  the  tricuspid  curtains. 

The  physical  signs  consist  of  a  presystolic  thrill  and  murmur,  a  right-sided  cardiac  en- 
largement, marked  cyanosis  and  a  presystolic  liver  pulsation.  An  intravitam  diagnosis 
is  rarely  made,  owing  to  the  similarity  of  the  physical  signs  with  those  of  mitral  obstruction. 
(After  Norris'  "Studies  in  Cardiac  Pathology.") 


All  these  rules  are  subject  to  exceptions  due  to  cardiac  displacement, 
etc.  Murmurs  themselves  are  variable  and  often  multiple  and^'compli- 
cated  by  pericardial  or  respiratory  sounds.  Occasionally  murmurs  [are 
subjectively  audible  to  the  patient  himself,  or  they  may  be  heard  by  the 
examiner  at  quite  a  distance  from  the  patient.  Both  of  these  statements 
apply  chiefly  in  case  of  certain,  loud,  high-pitched,  musical  murmurs. 


HEART    MURMURS 


237 


Fig.  203. — Mitral  stenosis.  This  lesion  generally  occurs  in  early  adult  life,  and  results 
from  rheumatic  endocarditis.  The  illustration  shows  enormously  thickened  and  contracted 
mitral  curtains,  thickened,  shortened  and  adherent  chorda?  tendinea?,  and  as  a  result,  a 
funnel-shaped  mitral  stenosis. 

The  most  characteristic  physical  signs  of  mitral  obstruction  are:  a  presystolic  thrill  and 
murmur  at  the  apex,  with  a  snappy  first  sound,  and  accentuation  of  the  pulmonary  second 
sound.  The  pulse  is  small  in  volume  and  frequently  irregular.  The  heart  enlarges  toward 
the  right. 


Fig.   204.— Illustrath 


od  flow  in  mitral  obstruction. 


238 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


V.A.M. 


R.B. 


R.P.A. 


B.L.N. 


I.V.C. 


Fig.  205. — The  right  heart  and  its  tributary  blood  channels.  Pulsation  is 
readily  transmitted  to  the  liver  either  (1)  directly  from  the  right  ventricle  or  (2)  indirectly,  as 
the  result  of  tricuspid  regurgitation,  the  inferior  vena  cava  being  short.  In]  the  latter 
instances  the  pulsation  instead  of  being  more  or  less  localized  to  the  epigastrium  is  general 
and  expansile  in  character.    The  liver  shows  sphygmographically  a  positive  venous  pulse. 

The  blood^pathway  from  the  jugular  veins  into  the  right  auricle  is  also  a  very  direct 
one,  hence  jugular  tracings  (phlebograms)  readily  depict  pressure  changes  in  the  auricle, 
especially  when  the  subject  is  recumbent  and  gravity  assists  in  the  stasis  of  venous  flow. 
R.B.,  right  bronchus;  R.P.A.,  right  pulmonary  artery;  B.L.N. ,  bronchial  lymph  node; 
L.A.,  left  auricle;  I.V.C,  inferior  vena  cava;  S.V.C.,  superior  vena  cava;  R.A.A.,  right 
auricular  appendage;  R. A.,  right  auricle;  .4. T.,  anterior  tricuspid  leaflet;  V.A.M.,  vena 
azygos  major. 


HEART    MURMURS 


239 


Pleural  1 
cavity 
filled  with 
serous  exu- 
date 


Comple- 
mental 
space   filled 
with 
[  exudate. 


Fig.  206. — Right-sided  hydrothorax.  Frozen  section  from  a  case  of  cardiac  anasarca 
similar  to  that  depicted  in  Figs.  211,  381.  Almost  the  entire  pleural  cavity  was  filled  with 
serous  effusion.  The  lung  which  was  completely  collapsed  and  compressed,  has  been  re- 
moved in  the  proximal  sections,  leaving  only  small  areas  in  this,  the  last  section  cut.  The 
heart  is  pushed  forward,  the  diaphragm  and  liver  downward.  The  inferior  vena'cava  is 
greatly  distended,  the  right  auricle  dilated.  The  liver  is  engorged  and  has  the  typical 
"nutmeg"  appearance.  The  complemental  space  anteriorly  and  posteriorly  was  filled 
with  fluid.  The  patient,  who  suffered  from  rheumatic  mitral  obstruction  and  insufficiency, 
and  tricuspid  insufficiency  with  auricular  fibrillation,  died  with  cyanosis,  orthopnea  and 
general  anasarca.  L. A.;  left  auricle;  R.A.,  right  auricle;  B,  bronchus;  P. A.,  pulmonary 
artery. 


240 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


FUNCTIONAL  MURMURS 

Murmurs  variously  referred  to  as  functional,  accidental,  inorganic, 
hemic  or  anemic  may  be  heard  over  the  heart,  the  arteries  or  the  veins. 
While  functional  murmurs  have  ceased  to  have  the  diagnostic  signifi- 
cance which  was  once  attached  to  them  their  recognition  is  still  of  some 
importance.  A  knowledge  of  the  conditions  under  which  they  may  be 
heard  and  their  characteristics  are  essential,  however,  in  order  that  they 
may  not  be  confused  with  murmurs  arising  from  anatomical  changes 
either  in  the  heart  or  the  blood-vessels.  Function  murmurs  are  common 
in  anemia,  in  postfebrile  asthenia,  in  exophthalmic  goitre  and  in  cardiac 
displacement. 


Fig.  207. — Mitral  and  tricuspid  insufficiency.  The  heart  is  enlarged,  as  is  also  the 
liver,  which  is  tender  and  which  pulsates.  The  dotted  areas  show  the  regions  over  which  the 
systolic  mitral  and  tricuspid  murmurs  are  heard. 


The  Heart. — Cardiac  murmurs  not  due  to  anatomical  changes  in  the 
valves  nor  to  disease  of  the  heart  muscle,  are  very  frequently  en- 
countered. As  a  rule  they  are  associated  with  conditions  in  which 
anemia  is  a  marked  feature,  such  as  chlorosis  or  secondary  anemia  due 
to  severe  infections,  either  acute  or  chronic.  Aside  from  the  fact  that 
they  are  definitely  associated  with  the  various  forms  of  anemia  and  that 
they  disappear  when  this  condition  is  relieved,  but  little  is  known  as  to 
their  causation. 

The  cardiac  murmurs  heard  in  anemia  have  certain  characteristics 
which,  as  a  rule,  serve  to  distinguish  them  from  murmurs  due  to  anatom- 
ical changes  in  the  heart. 


HEART    MURMURS 


241 


1.  They  are  definitely  associated  with  the  heart  and  while  they  may 
be  heard  at  any  one  of  the  valvular  orifices,  they  are  most  frequently 
encountered  over  the  pulmonary  area,  at  the  second  costal  cartilage  or 
third  interspace  on  the  left.  Next  to  the  pulmonary  area  the  region  of 
the  apex  of  the  heart  is  the  most  frequent  site.  Occasionally  a  functional 
murmur  is  heard  over  the  aortic  and  tricuspid  areas. 

2.  They  are  not  transmitted  but  are  sharply  localized. 

3.  They  are  always  systolic  in  time,  but  often  terminate  before  the 
end  of  systole. 

4.  They  are  frequently  associated  with  a  functional  murmur  either 
in  the  veins  or  the  arteries. 


Fig.  208. — Functional  murmurs.     Showing  relative  frequency  of  occurrence  over  different 
areas  of  the  precordium;  1,  being  the  most  frequent  site. 


5.  They  are  uniformly  low-pitched;  the  sound  is  soft  in  character, 
and  variable  in  quality  and  intensity.  The  sound  produced  by  a  func- 
tional murmur  never  has  the  rough  or  occasional  musical  quality  of  an 
organic  murmur.  At  times  a  functional  murmur  is  loudest  when  the 
patient  is  in  the  recumbent  posture  and  in  some  cases  this  is  the  only 
position*  in  which  it  can  be  elicited.  The  murmur  is  apt  to  be  loudest 
immediately  after  lying  down,  before  the  vessels  have  accommodated 
themselves  to  the  change  in  gravity.  The  murmur  may  be  intensified 
by  violent  cardiac  action  due  either  to  nervous  excitement  or  exertion. 

Transitory  Murmurs  Due  to  Exertion. — Accidental  murmurs  ap- 
parently endocardial  in  origin  are  frequently  developed  as  the  result  of 
violent  exertion.  They  are  very  transitory  and  are  rarely  heard  beyond 
a  few   minutes  succeeding  the  exertion.     In   an  examination   of   1552 

16 


242 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


students  at  Cornell  University,  Munford  encountered  murmurs  of  this 
character  in  117,  or  7.48  per  cent.,  after  the  student  had  been  required 
to  "chin"  himself  as  often  as  possible.1  They  are  generally  ascribed  to 
loss  of  muscle  tone  affecting  chiefly  the  mitral  sphincter  and  hence  are 
more  common  in  individuals  who  are  not  "in  training." 

Functional  murmurs  are  very  easily  produced.  The  vascular^dila- 
tation  induced  by  prolonged  sweat  baths  is  of  itself  sufficient  to  cause  the 
appearance  of  murmurs  in  the  majority  of  cases.2 


Fig.  209. — Pulmonary  obstruction,  or  dilatation.  Indicating  the  area  over  which 
systolic  pulmonary  murmurs  are  heard,  with  a  diagrammatic  illustration  of  the  relationship 
between  the  murmur  and  the  heart  sounds. 


THE  EFFECT  OF  RESPIRATION  ON  ENDOCARDIAL  MURMURS 

1.  Inspiration  causes  the  lungs  to  overlap  the  heart  and  thus  tends 
to  make  murmurs  more  feeble. 

2.  Inspiration  favors  blood  flow  into  and  out  of  the  right  heart. 
During  rapid  breathing  it  hinders  blood  flow  in  the  left»heart,  by  retain- 
ing more  in  the  lungs.  During  slow  breathing  this  effect  is  only  manifest 
during  the  first  half  of  the  act,  because  in  the  last  half  the  pulmonary 
vessels  dilate  no  further. 

3.  Expiration  acts  in  the  reverse  manner,  hindering  blood  flow  in 

1  R.  T.  McKenzie  found  that  among  266  apparently  healthy  students  74  (27.8  per 
cent.)  developed  cardiac  murmurs  under  vigorous  exercise.  Of  these  35  were  of  the 
pure  pulmonic  systolic  type.  If  the  cases  are  included  in  which  this  murmur  occurred 
in  association  with  other  murmurs  it  was  present  in  64  cases,  only  10  men  out  of  the 
74  failing  to  show  it.  Murmurs  were  slightly  more  common  among  the  non-athletic 
students.  These  functional  murmurs  were  more  frequent,  more  intense  and  some- 
times present  only  in  recumbency. 

2  Howell,  F. :  "Physiological  Heart  Murmurs  Produced  by  Electric  Light  Baths." 
Boston  Med.  &  Surg.  Jour.,  April  3,  1902. 


HEART    MURMURS 


243 


the  right  and  favoring  it  in  the  left,  especially  with  rapid  or  forced  breath- 
ing. These  facts  may  be  used  to  help  in  the  differentiaton  of  right-  or 
left-sided  valvular  lesions. 


Fig.  210. — Aortic  and  mitral  insufficiency.  Aortic  and  mitral  insufficiency  with  left 
ventricular  hypertrophy  and  dilatation,  also  a  small  pericardial  effusion. 

The  aortic  valves  are  shrivelled  and  retracted,  the  left  ventricle  is  hypertrophied  and 
dilated,  this  dilatation  affecting  the  mitral  orifice.  The  apex  impulse  is  displaced  down- 
ward and  to  the  left.  T,  trachea;  A,  aorta;  P. A.,  pulmonary  artery;  L.A.A.,  left  auricular 
appendage;  M.L.,  mitral  leaflets  ;P,  pericardial  sac;  S.V.,  subclavian  vessels;  S.V.C.,  superior 
vena  cava;  A.L.,  aortic  leaflets;  R.A.,  right  auricle. 

Physical  signs:  A  heaving  impulse,  a  booming  first  sound,  a  systolic  mitral  murmur 
transmitted  to  the  axilla.  A  faint,  low-pitched  aortic  diastolic  murmur  transmitted  toward 
the  cardiac  apex  and  to  the  ensiform  cartilage.  Pulmonic  second  sound  accentuated.  Pul- 
sating carotid  and  brachial  arteries,  a  water-hammer  pulse,  Duroziez's  murmur,  blood- 
pressure:  systolic  180,  diastolic  55  nam.  Hg. 

SPECIAL  VARIETIES  OF  MURMURS 

Duroziez's  Murmur. — If  the  femoral  artery  be  slightly  indented  by 
pressure  of  the  stethoscope  during  auscultation,  a  systolic  murmur  will 
be  heard  which  results  from  vibration  of  the  vessel  walls  due  to  the  local 
constriction  of  the  blood  stream.  In  aortic  insufficiency,  where  blood 
flow  is  rapid  and  where  the  current  flows  alternately  forward  and  back- 
ward, a  doable  murmur  may  be  heard  over  the  femoral  artery.  This 
is  known  as  Duroziez's  murmur.     It  is  not  pathognomonic  of  aortic  in- 


244 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


sufficiency  but  may  "occur  in  other  conditions  associated  with  vasomotor 
relaxation. 

Traube's  Sound. — In  some  cases  of  aortic  insufficiency  with  marked 
hypertrophy  and  a  large  systolic  output,  the  sudden  distention  of  the 
arteries  produces  a  cracking  noise  known  as  a  pistol-shot  sound.  This 
may  be  heard  even  in  the  absence  of  aortic  insufficiency  if  the  pulse  pres- 
sure be  large,  and  the  diastolic  pressure  low.  In  some  cases  of  aortic 
and  tricuspid  insufficiency  a  double  sound  of  this  character  may  be  heard 
over  the  femoral  vessels.  This  has  been  shown  to  consist  of  a  venous  as 
well  as  an  arterial  element.  It  is  due  to  sudden  distention  of  the  femoral 
artery,  and  to  sudden  backward  pressure  upon  the  femoral  venous  valves. 


Skodaic  tympany,  exag- 
gerated breath  sounds, 
crackling  rales. 

Dulness,  feeble  breath 
sounds,  fremitus  and 
vocal   resonance. 

Flatness 

Pulsating  liver  tender- 
ness. 


Bulging    flanks,    succus- 
sion  wave. 


Pulmonic    second   sound 
loud. 


Apex  impulse  displaced, 

downward  and    outward 

arrhythmia. 

Systolic  murmur  replaces 

first  sound. 


Pitting  of  the  abdominal 
wall,  edema  of  arms, 
glossy  skin. 


Fig.  211. — Cardiac  dropsy.  A  case  of  general  dropsy  (anasarca)  following  dilata- 
tion of  the  heart,  due  to  mitral  and  tricuspid  disease.  Orthopnea,  cyanosis,  right-sided 
hydrothorax,  passive  congestion  of  the  lungs,  liver  and  spleen,  ascites,  etc.  The  patient,  a 
girl  of  fourteen  years,  shows  emaciation  and  retarded  development  due  to  the  cardiac 
lesion.  Also  pitting  of  the  abdominal  wall  due  to  subcutaneous  edema.  A  character- 
istic picture  of  broken  cardiac  compensation  with  tricuspid  insufficiency  is  presented. 


The  latter  element  precedes  the  former  because  the  blood  from  the  leak- 
ing tricuspid  valve  begins  to  regurgitate  during  the  period  of  valvular 
closure  (beginning  of  systole)  while  the  arterial  distention  does  not  take 
place  until  the  end  of  this  period.1 

The  Flint  Murmur. — This  murmur  is  presystolic  in  time;  it  is  best 
heard  within  and  above  the  cardiac  apex.  It  occurs  in  some  cases  of 
aortic  insufficiency.  There  has  been  much  dispute  about  its  etiology 
and  significance,  but  it  is  generally  believed  to  be  due  to  the  flapping 
of  the  anterior  mitral  curtain  between  two  blood  streams,  i.e.,  between  the 

^chultze:  Deut.  Med.  Woch.,  1905,  xxxv. 


HEART    MURMURS 


245 


normal  flow  from  the  left  auricle  and  the  regurgitant  flow  from  the 
aortic  leaflets  into  the  left  ventricle.  Hirschfelder  has  shown  that  in  the 
excised  heart,  if  the  ventricular  pressure  is  increased,  the  mitral  valve 
opens  only  along  part  of  its  line  of  closure,  and  that  therefore  an  actual 
functional  stenosis  may  exist.  The  importance  of  this  murmur  lies  in 
the  fact  that  it  may  present  the  exact  acoustic  phenomena  of  organic 
mitral  stenosis.  It  may  be  differentiated  from  the  last-named  condition 
by  the  fact  that  it  is  not  associated  with  a  marked  presystolic  thrill,  an 


Fig.  212. — The  Flint  murmur.  The  aortic  and  the  mitral  valves  are  contiguous 
structures.  The  Flint  (presystolic)  murmur  is  produced  by  the  regurgitation  of  blood 
through  the  aortic  orifice.  The  curtains  of  the  mitral  valve  are  caught  between  two  blood 
currents — that  just  mentioned  and  that  streaming  in  from  the  left  auricle — and  flap  like  a 
loose  sail  in  the  wind. 


enlarged  right  heart,  a  snappy  first  sound  and  a  small,  well-sustained 
pulse.  The  Flint  murmur  is  found  in  conjunction  with  other  signs  of 
aortic  insufficiency  such  as:  a  pulse  which  is  large  in  volume  and  col- 
lapsing in  type — the  diastolic  pressure  being  low  and  the  pulse  pressure 
large;  left  ventricular  hypertrophy  and  the  vascular  and  pulsatory 
phenomena  so  characteristic  of  an  incompetent  aortic  valve1  (see  Fig.  212). 

1  The  relative  frequency  of  pulsatory  phenomena  in  124  cases  of  aortic  insufficiency 
was  found  to  be  as  follows:  Corrigan  pulse  95  per  cent,,  capillary  pulse  90  per  cnii.. 
Duroziez  murmur  88  per  cent.,  visible  arterial  pulsation  76  per  cent.,  femoral  snap 
45  per  cent.,  Traube's  sign  24  per  cent.,  visible  venous  pulse  7  per  cent.  (Tice). 


246  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

Roger's  murmur  is  sometimes  heard  in  cases  of  patulous  inter- 
ventricular septum.  It  is  continuous  throughout  systole  and  diastole 
with  an  ictus  or  reinforcement  during  the  former.  It  has  a  rhythmic, 
somewhat  musical  character  with  a  periodic  intensification  like  the 
whirring  of  a  foot-propelled  knife-grinder's  wheel.  It  is  best  heard  in 
the  upper  third  of  the  precordium  over  the  median  portion  of  the  septum 
itself.  It  is  not  transmitted  but  gradually  fades  out  in  all  directions  as 
the  point  of  maximum  intensity  is  receded  from.  Phonetic  equivalent: 
Whir  -r  -r  -r  -r  (Fig.  88,  I). 

EXO CARDIAL  MURMURS 

In  the  large  arteries  near  the  heart  (subclavian,  etc.)  certain  sounds 
may  be  faintly  heard.  They  may  be  due  to:  (1)  stretching  and  vibra- 
tion of  the  vessel  walls,  or  to  (2)  conduction  of  the  second  heart  sound. 
In  the  distant  arteries  one  may  have  murmurs  from  stethoscopic  pres- 
sure, or  murmurs  conducted  from  the  aortic  orifice,  etc.  Very  often  a 
systolic  murmur  is  heard  over  the  vertex  of  the  skull  of  children  from 
the  third  month  to  the  sixth  year.     It  is  without  significance. 

Systolic  murmurs  in  arteries  may  be  due  to:  (a)  roughening  of  the 
intima;  (fc)  narrowing  of  lumen;  (c)  dilatation — fevers,  vasomotor  par- 
esis; (d)  aneurism. 

Subclavian  murmurs  are  generally  short  in  duration  and  always 
systolic  in  time.  Often  a  harsh  systolic  whiff  is  heard,  especially  during 
inspiration,  generally  on  the  left  side,  and  most  commonly  in  men  at 
the  junction  of  the  middle  with  the  outer  third  of  the  clavicle.  The 
murmur  is  increased  by  deep  inspiration,  sometimes  audible  only  during 
forced  inspiration  and  modified  by  the  position  of  the  arm.  It  may 
be  inconstant.  Subclavian  murmurs  possess  no  pathologic  significance; 
they  are  generally  due  to  constriction  of  the  artery  between  the  clavicle 
and  the  first  rib,  although  a  similar  constriction  may  be  produced  by 
fibroid  disease  of  the  pleura.  Hence  they  are  frequently  encountered  in 
cases  of  pulmonary  tuberculosis.  Landis  found,  among  31  cases  studied, 
that  the  murmur  was  associated  with  pulmonary  tuberculosis  in  20. 
The  fact  that  the  murmur  is  heard  more  frequently  on  the  left  than  the 
right  side,  even  in  cases  in  which  the  pulmonary  disease  is  more  extensive 
on  the  right  side,  suggests  that  the  real  explanation  lies  in  some  anatomi- 
cal variation  of  the  two  arteries.  Furthermore,  subclavian  murmurs 
have  been  frequently  noted  in  individuals  healthy  in  every  respect. 
While  probably  of  but  little  importance  the  presence  of  a  subclavian 
murmur  should  suggest  a  careful  examination  of  the  apices  of  the  lungs. 

Carotid  Murmurs. — Systolic  murmurs  heard  in  the  carotid  arteries, 
especially  the  right,  are  not  uncommon.  As  a  rule  the  murmur  is  trans- 
mitted, having  its  origin  in  disease  of  the  aortic  leaflets  (stenosis  or 
roughening)  or  in  disease  of  the  first  part  of  the  aorta  (roughening  from 
atheromatous  plates  or  slight  dilatation).  The  latter  conditions  are  by 
far  the  most  frequent  sources  of  the  murmur.  Occasionally  a  systolic 
murmur,  due  to  anemia,  is  heard  in  the  carotids.  An  aneurism  may 
produce  a  similar  murmur. 

Accidental  murmurs  are  frequently  heard  over  the  enlarged  thyroid 
gland  in  exophthalmic  goitre.  They  may  be  systolic  or  diastolic  in 
time. 


HEART    MURMURS  247 

VENOUS  MURMURS 

Venous  murmurs  (bruit  de  diable,  nun's  murmur,  souffle,  venous  hum) 
were  formerly  considered  an  indication  of  anemia.  They  consist  of  soft, 
low-pitched  continuous  humming  sounds  of  variable  quality  and  inten- 
sity with  a  rhythmic  accentuation.  They  are  heard  in  the  large  veins 
above  the  clavicles  in  50  per  cent,  of  all  children.  They  are  loudest 
during  auricular  diastole  (faster  flow) ,  in  the  erect  or  sitting  postures,  and 
on  the  right  side  behind  the  lower  margin  of  the  sternomastoid  muscles. 
The  right  internal  jugular  vein  is  almost  a  linear  continuation  of  the  right 
innominate  vein,  the  internal  jugular  is  held  open  by  the  cervical  fascia 
and  hence  cannot  diminish  in  calibre  when  the  amount  of  blood  lessens; 
hence  a  fluid  vein  is  produced  and  a  murmur  results.  The  condition  is 
increased  by  hydremia  (anemia). 

Another  explanation  is  that  based  on  a  constriction  of  the  vein. 
"By  having  the  patient  turn  the  head  upward  and  away  from  the  side 
auscultated  the  internal  jugulars  are  made  tense  and  compressed  against 
the  transverse  processes  of  the  lower  cervical  vertebrae  with  which  they 
are  in  relation.  In  this  way  the  calibre  of  the  vein  is  narrowed  and  the 
flow  of  blood  accelerated."1  Many  explanations  as  to  the  exact  cause 
of  venous  hums  have  from  time  to  time  been  offered.  None  are  invariably 
satisfactory.  The  diagnostic  value  of  venous  murmurs  from  any  standpoint 
is  very  slight. 

It  is  said  that  a  venous  hum  may  be  heard  in  the  femoral  veins  under 
the  same  conditions  in  which  it  is  heard  in  the  jugulars,  but  we  have 
never  been  able  to  verify  this  statement. 

Eustace  Smith's  Sign. — Occasionally  a  venous  hum  is  heard  over  the 
sternum  just  beneath  the  notch.  The  murmur  is  elicited  by  tilting  the 
head  back  and  is  supposedly  produced  in  the  left  innominate  vein,  which 
passes  from  left  to  right  with  a  slight  obliquity  downward  behind  the 
upper  part  of  the  sternum,  by  reason  of  the  vein  being  pressed  upward 
by  enlarged  bronchial  lymph  nodes.  This  explanation  appears  to  be 
erroneous.  The  bronchial  lymph  nodes  at  the  bifurcation  of  the  trachea 
are  too  far  above  the  heart  to  cause  .pressure  on  the  large  vessels.  The 
pressure  is  probably  caused  by  an  enlarged  persistent  thymus  gland 
(Gittings).  When  the  murmur  is  present  over  the  sternum  it  is  also 
heard  in  the  jugulars,  where  in  all  probability  it  originates. 

Although  frequently  referred  to  as  a  sign  of  some  value  in  the  recogni- 
tion of  enlarged  bronchial  lymph  nodes  in  children,  we  have  rarely  been 
able  to  elicit  it  even  in  cases  in  which  there  were  other  signs  pointing 
strongly  to  this  condition. 

CARDIO-RESPIRATORY  MURMURS 

(Cardio-pulmonary,  cardio-pneumatic,  systolic  vesicular  murmurs.) 
Cardio-respiratory  murmurs  are  interrupted  or  abnormal  breath 
sounds  produced  by  the  movement  of  the  heart  upon  the  surrounding 
lung  tissue.  The  respiratory  sounds  may  be  interrupted  by  a  series  of 
periodic  interruptions  or  increments  of  intensity  (puffs  or  "cogs")  which 
may  be  heard  even  when  the  breath  is  held.  They  often  vary  with  the 
cardiac  or  respiratory  rate  and  phase.     They  are  generally  loudest  near 

1  Landis  and  Kaufman:  Arch.  Pediatrics,  Feb.  12,  1912. 


248 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


the  cardiac  apex  and  along  the  left  border  of  the  heart,  but  they  may  be 
heard  along  the  right  border,  in  the  scapular  region  and  elsewhere.  They 
are  influenced  by  respiration,  being  generally  louder  during  deep  inspira- 
tion. They  are  apt  to  be  affected  by  change  of  posture;  they  generally 
disappear  in  recumbency,  and  nearly  always  during  apnea.  They  are 
not  accurately  synchronous  with  the  heart,  but  often  appear  in  the  middle 
of  systole,  being  distinctly  separated  from  the  first  sound.  They  often 
begin  and  end  suddenly,  are  sharply  localized  and  seem  close  to  the  ear 
of  the  examiner.  They  are  not  transmitted  in  the  directions  which  are 
characteristic  of  endocardial  murmurs.  They  are  often  intermittent, 
associated  with  rales,  and  influenced  by  stethoscopic  pressure.  They 
may  occur  in  perfectly  normal  individuals,  but  are  especially  common  in 
pulmonary  tuberculosis,  especially  when  the  pleura  has  been  extensively 
involved,  and  in  atelectatic  lungs,  as  well  as  in  patients  who  have  had 
pleuritis  or  pneumonia,  or  in  those  suffering  from  paroxysmal  tachy- 
cardia. 


Fig.  213.  Fig.  214. 

Figs.  213  and  214. — The  distribution  of  cardio-respiratory  murmurs  in  48  cases.  Com- 
posite pictures  "constructed  by  shading  the  affected  area  of  each  chest  upon  the  same 
diagram  by  lines  approximately  equidistant."  The  actual  numerical  frequency  is  shown 
by  the  attached  leaders.      {After  Thomas  Lewis,  Quart.  Jour.  Med.,  Jan.,  1909.) 

Gerhartz  has  shown  that  cardiac  murmurs  are  generally  due  to 
vibrations  of  about  the  same  rate  as  those  which  correspond  to  the  lower 
range  of  the  respiratory  sound' (60  to  80  vibrations  per  second).  The 
fact  that  the  two  types  of  sound  have  about  the  same  pitch  accounts  for 
the  difficulty  which  sometimes  attends  their  differentiation.  Cardio- 
respiratory murmurs  have  no  pathologic  significance  except  that  they  may 
indicate  pleural  adhesions;  their  importance  merely  lies  in  the  fact  that 
they  may  be  mistaken  for  endocardial  murmurs  or  pericardial  frictions. 

Succussion  splash  synchronous  with  the  heart  may  be  heard  in  the 
neighborhood  of  the  precordium.  It  is  generally  produced  in  the  stom- 
ach, although  it  may  be  due  to  hydropneumothorax,  or  to  hydropneumo- 
pericardium. 

Hepatic  murmurs  may  be  heard  over  the  liver  or  in  the  epigastrium 
in  some  (rare)  cases  of  hepatic  cirrhosis.  They  are  generally  venous  in 
origin  (blood  flowing  from  small  into  larger  veins,  or  sinuses)  and  maybe 
continuous  or  intermittent  in  character. 


HEART    MURMURS 
PERICARDIAL  FRICTION  SOUNDS 


249 


In  the  early  stages  of  pericarditis  the  serous  membrane  which  is  nor- 
mally smooth  and  moist  becomes  roughened  as  a  result  of  congestion  and 
exudation.     The  exudate  which  occurs,  instead  of  noiselessly  gliding  over 


Fig.  215. — Acute  sero-fibrinous  pericarditis.  The  pericardial  sac  is  stretched  and  has 
been  greatly  distended  by  serous  exudate.  Both  the  mural  and  the  visceral  surfaces  arc 
covered  with  fibrinous  exudate  (cor  villosum,  bread  and  butter  pericardium).  Such  a  heart 
would  yield  loud  friction  sounds  in  the  early  stages  of  inflammation.  Later  when  the 
serous  surfaces  were  separated  by  liquid  effusion  the  friction  would  disappear,  except  per- 
haps at  the  base,  while  the  heart  sounds  would  be  muffled  and  distant.  (From  Norris' 
"Cardiac  Pathology.") 

the  neighboring  pericardium,  now  produces  a  rough,  scratching  or  scrap- 
ing sound,  similar  in  quality  to  that  heard  over  an  inflamed  pleura.  This 
sound  is  known  as  a  pericardial  friction.  It  often  has  a  dry,  creaking 
or  shuffling,    leathery   quality,  is  heard   during  both  systole  and  diastole, 


250 


THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 


and  is  therefore  described  as  being  "to  and  fro."  It  is  frequently  ac- 
companied by  local  pain,  seems  close  to  the  ear  and  is  intensified  by  pres- 
sure. It  remains  localized,  is  not  transmitted  in  the  directions  character- 
istic of  endocardial  murmurs,  and  is  often  loudest  over  the  middle  of  the 
precordium  where  the  heart  is  uncovered  by  lung  tissue.  It  may  be  dif- 
ferentiated (1)  from  a  pleural  friction  by  the  fact  that  it  is  synchronous 
with  the  heart,  and  not  with  respiration  and  that  it  does  not  disappear 
during  the  Valsalva  experiment;  and  (2)  from  endocardial  sounds,  by  the 


Fig.  216. — Pericardial  effusion:  the  body  being  frozen  in  the  recumbent  posture  and 
viewed  from  behind.  The  heart  is  hypertrophied  and  dilated.  Both  lower  pulmonary 
lobes  are  compressed,  the  left  by  the  effusion,  the  right  by  the  congested  liver  which  has 
been  forced  upward  as  the  result  of  ascites  (recumbent  posture).  The  physical  findings 
are  shown  in  Fig.  217.      (Compare  Figs.  175,  358,  359.) 


fact  that  it  is  not  accurately  synchronous  with  either  systole  or  diastole, 
but  often  overlaps  them  both  because  the  greatest  systolic  excursion  of 
the  cardiac  surface  corresponds  to  the  expulsion  time  and  not  to  either 
systole  or  diastole.  A  further  difference  lies  in  the  fact  that  the  friction 
tends  to  vary  in  quality  and  intensity  not  only  in  the  course  of  a  few 
hours,  but  even  at  times  from  one  heart  beat  to  another.  Leaning  for- 
ward or  lying  on  the  left  side  tends  to  intensify  the  sound  while  the  right 


HEART    MURMURS 


251 


lateral  decubitus  often  diminishes  it.     The  pericardial  friction  may  have 
a  shuffling  triple  rhythm  very  similar  to  gallop  rhythm. 

Pericardial  Effusion. — Unless  the  pericardial  inflammation  is  promptly 
arrested,  the  exudate  poured  out  into  the  pericardial  sac  increases  and 
becomes  more  liquid  in  character — serum,  pus  or  blood.  Such  a  peri- 
cardial effusion  muffles  the  heart  sounds  so  that  they  become  feeble  or 
even  inaudible.  Under  such  circumstances  the  friction  sound  disappears. 
Such  a  condition  is  associated  with  an  increase  of  heart  dulness,  which 
forms  an  obtuse  cardio-hepatic  angle.  The  inflammation  and  effusion 
cause  a  softening  and  distention  of  the  pericardium,  which  in  some  cases 
may  become  so  large  as  to  simulate  a  pleural  effusion  and  may  produce 
compression  of  the  left  lung  with  associated  dulness  and  bronchial  breath- 


Exaggerated    breath 

sounds,  scattered 
rales 


Muffled  breath 
sounds,  distant  bron- 
cho-vesicular 
breathing 
(small  pleural 
effusion) 


To  and  fro  friction 
sound, synchronous 
with  the  heart 

Apex  impulse  feerjle, 
sounds  muffled,  a 
distant  systolic  mur- 
mur is  heard 


Fig.  217. — Percussion  outlines  in  case  whose  heart  is  depicted  in  Fig.  215.  The  heart 
dulness  isyery  large  and  merges  with  that  of  the  liver;  it  is  somewhat  pyriform  in  shape. 
The  cardiohepatic  angle  is  obtuse.  The  abdomen  is  distended  and  bulges  in  the  flanks 
(ascites).  The  patient  suffers  from  orthopnea — the  shoulders  are  raised  and  the  accessory 
muscles  of  respiration  brought  into  play.  The  breath  sounds  were  harsh  and  exaggerated 
and  associated  with  crackling  rales  (congestion).  The  scar  between  the  umbilicus  and 
pubis  results  from  paracentesis  abdominalis. 


ing.  In  children,  bulging  of  the  precordium  may  occur.  Cardiac  dul- 
ness extends  further  to  the  left  beyond  the  apex  impulse  than  is  the  case 
in  hypertrophied  hearts.  Dulness  in  the  fifth  right  intercostal  space 
near  the  sternum  (Rotch's  sign)  is  sometimes  demonstrable  quite  early 
in  the  effusion  stage.  Stress  is  sometimes  laid  upon  the  fact  that  the 
heart  dulness  in  pericardial  effusions  tends  to  be  pyriform,  but  this  is 
certainly  not  always  the  case.  An  area  of  percussion  dulness  at  the 
angle  of  the  left  scapula  together  with  bronchial  breathing,  etc.,  is  some- 
times due  to  pressure  of  a  large  pericardial  effusion  upon  a  portion  of 
the  lung  {Ewarl's  sign). 


252  THE    EXAMINATION"    OF    CIRCULATORY    SYSTEM 

Changing  the  patient's  posture  from  the  erect  to  the  right  lateral 
position  tends,  in  pericardial  effusion,  to  produce  a  greater  displacement 
of  the  heart  to  the  right  than  is  the  case  in  simple  hypertrophy. 

Progressive  enfeeblement  of  the  heart  sounds,  especially  when  a 
friction  sound  has  been  heard  or  suspected,  may  have  distinct  diagnostic 
value. 

It  should  be  remembered  that  small  pericardial  effusions  are  fre- 
quently overlooked  and  it  has  been  stated  that  no  effusion  is  demon- 
strable by  physical  signs  until  it  amounts  .to  150  c.c.  (see  Figs.  358- 
63  inch). 


Fig.  218. — Pericardial  adhesions.  The  illustration  shows  dense,  localized,  fibrous 
adhesions  near  the  apex  of  the  heart  (which  is  dilated),  the  result  of  antecedent  pericardial 
inflammation.  Such  a  condition  is  suggested  by  localized  systolic  retraction  of  the  chest 
wall,  especially  if  associated  with  diminished  postural  mobility  of  the  heart,  with  symptoms 
of  cardiac  insufficiency  out  of  proportion  to  the  demonstrable  physical  signs,  lack  of  response 
to  the  usual  methods  of  treatment  (digitalis,  rest,  etc.),  especially  if  coupled  with  a  history 
of  a  previous  attack  of  rheumatic  fever  or  pneumonia.  {From  Norris'  "Cardiac  Path- 
ology.") 

An  X-ray  examination  may  throw  much  useful  light  upon  doubtful 
cases. 

There  is  considerable  variation  regarding  the  position  of  the  heart  in 
pericardial  effusions,  as  well  as  difference  of  opinion  regarding  its  cause. 
It  seems  that  the  position  depends  upon  the  size  of  the  heart,  which  in 
turn  depends  upon  the  amount  of  blood  it  contains,  which  is  in  turn  de- 
termined by  the  stage  of  compensation.  When  the  heart  is  well  filled 
with  blood  its  position  is  relatively  normal,  but  when  it  is  small  and  partly 
collapsed  it  may  fall  backward  against  the  posterior  pericardial  wall;  the 
apex  being  more  or  less  displaced  toward  the  right.     Occasionally  it  may 


HEART    MURMURS  253 

remain  in  an  anterior  position,  in  which  it  is  maintained  by  the  elasticity 
of  the  great  vessels. 

Effusions  amounting  to  750  c.c.  may  be  sufficient  to  cause  the  dis- 
appearance of  all  friction  sounds  even  at  the  base,  but  on  the  other  hand 
a  friction  may  persist  with  effusions  of  1000  c.c.  or  more. 

Pleuro-pericardial  sounds  are  due  to  roughening  of  the  external  sur- 
faces of  the  pleura  and  the  pericardium.  They  are  heard  best  at  the  left 
anterior  pulmonary  border,  are  often  affected  by  respiration,  posture,  etc. 

PRACTICAL  CONSIDERATIONS 

In  examining  the  heart,  observations  should  always  be  made  in  both 
the  erect  and  in  the  recumbent  posture.  The  results  thus  obtained  are 
often  variable,  and  physical  signs  absent  in  one  position  may  be  readily 
demonstrable  in  the  other.  When  the  findings  are  recorded,  the  position 
should  be  stated. 

In  the  erect  posture  the  apex  beat  is  lower,  the  cardiac  dulness  is  less- 
ened, the  aortic  second  sound  is  louder  than  the  pulmonic  (after  twenty- 
five  years  of  age),  the  splitting  of  the  second  sound  if  previously  present 
tends  to  disappear;  the  murmurs  of  aortic  insufficiency  and  mitral  ob- 
struction become  louder,  as  does  also  the  venous  vascular  hum. 

In  recumbency  the  apex  beat  is  higher,  the  cardiac  dulness  is  generally 
more  marked,  the  pulmonic  second  sound  louder  than  the  aortic,  even 
in  adults.  Reduplication  of  the  second  sound  is  often  present;  the  mur- 
murs of  mitral  insufficiency,  tricuspid  insufficiency,  aortic  obstruction, 
and  most  functional  murmurs  become  more  intense.  The  differences 
are  chiefly  due  to  the  effects  of  gravity  upon  the  position  of  the  heart  and 
upon  the  blood  flow. 

It  is  often  advisable  to  have  the  patient  indulge  in  some  form  of  exer- 
cise, provided  his  physical  condition  permits  of  it,  such  as  climbing  a 
flight  of  stairs,  or  "dipping"  (touching  the  floor  with  the  finger  tips,  by 
flexion  of  the  knees  and  thighs).  These  procedures  will  often  develop 
latent  murmurs,  irregularities  or  cardiac  erythism.  It  is  always  well, 
especially  in  high-strung  individuals,  to  count  the  pulse  while  the  patient 
is  resting  quietly,  before  the  clothes  have  been  removed,  and  to  repeat 
both  the  pulse  count  and  the  blood-pressure  estimation  at  the  end  of  the 
examination,  after  the  patient  has  become  tranquilized. 

It  should  be  borne  in  mind  that  functional  murmurs  are  of  frequent 
occurrence,  and  that  organic  heart  murmurs  are  nearly  always  accom- 
panied by  demonstrable  cardiac  enlargement,  increased  pulse  rate  or 
other  abnormalities.  Further  that  "a  disease  of  the  valves  is  not  a  dis- 
ease of  the  heart";  in  other  words  as  long  as  the  myocardium  is  healthy 
the  prognosis  is  relatively  good  regardless  of  valvular  leakage  or  ob- 
struction. 

Regarding  blood-pressure  estimations  we  should  bear  in  mind  that  the 
initial  reading  is  often  fallaciously  high,  especially  in  patients  unused  to 
this  examination.  Subsequent  examinations  made  after  the  patient  has 
learned  the  harmless  and  painless  nature  of  the  procedure  are  much  more 
accurate.  In  these  "psychic"  elevations,  however,  the  diastolic  pressure 
is  practically  unaffected,  even  when  the  systolic  pressure  has  been  tem- 
porarily elevated  15  or  20  mm.  Hg.  Systolic  pressures  above  160  mm. 
and  diastolic  readings  above  100  mm.  Hg  arc  abnormal  at  any  age.     The 


254  THE    EXAMINATION    OF    CIRCULATORY    SYSTEM 

most  frequent  cause  of  persistent  arterial  hypertension  is  chronic  glo- 
merulo-nephritis.  An  examination  of  the  urine  is  always  essential  since 
the  cardiorenal  relationship  is  a  close  and  important  one. 

An  examination  of  the  thyroid  gland  will  often  explain  cardiac  ab- 
normalities such  as  tachycardia,  hypertrophy,  dyspnea  and  lability  of 
the  pulse  and  of  blood-pressure.  Slight  edema  of  the  extremities  at  the 
end  of  the  day  point  to  cardiac  fatigue  and  insufficiency.  The  possible 
presence  of  an  aortic  aneurism  should  always  be  borne  in  mind,  in  patients 
who  complain  of  precardial  pain,  oppression,  cough,  dyspnea  or  other 
cardiac  or  respiratory  symptoms  without  evident  cause. 

Upon  discovering  the  existence  of  a  murmur  the  examiner  should 
determine  (1)  the  area  over  which  it  is  loudest;  (2)  its  time  in  relation 
to  the  cardiac  cycle;  (3)  the  direction  in  which  it  is  transmitted;  (4)  its 
character  and  constancy  in  relation  to  respiration,  posture  and  exercise. 
It  must  be  remembered  that  many  entirely  normal'  persons  may  present 
murmurs. 

The  effect  of  deep  forced  inspiration  and  expiration,  each  act  being 
held  for  a  number  of  seconds,  should  be  noted.  Functional  and  cardio- 
respiratory murmurs  will  be  much  affected  by  these  procedures  and  may 
indeed  disappear  entirely  during  one  or  the  other  phase.  Organic 
murmurs  are  much  less  or  not  at  all  affected.  Furthermore,  individuals 
with  organic  lesions  generally  cannot  hold  their  breath  as  long  as  normal 
people  without  discomfort,  distention  of  the  jugular  veins  or  cyanosis. 
The  effect  of  change  of  posture  from  the  erect  to  the  recumbent  position, 
and  of  exercise  such  as  dipping,  should  always  be  noted  not  only  in 
regard  to  the  murmur  but  also  upon  the  pulse  rate,  respiration  and  blood- 
pressure.  The  less  marked  and  the  more  brief  the  changes  produced, 
the  less  serious  generally,  the  lesion.  If  the  pulse  rate  remains  high  and 
the  blood-pressure  falls  after  moderate  exercise,  the  individual  is  at  least 
not  in  good  training,  and  people  with  organic  lesions  naturally  show  the 
effect  of  a  lack  of  it  more  than  those  with  normal  hearts. 

Functional  heart  murmurs  are  never  diastolic  in  time,  they  are  not 
accompanied  by  other  abnormalities  such  as  hypertrophy,  accentua- 
tion of  the  second  sounds,  arrhythmia,  cyanosis,  edema,  etc.,  and  they 
generally  occur  at  the  pulmonary  area — the  "region  of  romance"  of 
Balfour. 

Functional  murmurs  are  not  conducted  in  the  same  direction  nor  to  the 
degree  as  organic  murmurs.  Thus  a  mitral  systolic  murmur  if  conducted 
to  the  angle  of  the  scapula  may  be  considered  not  only  organic  but  the 
result  of  a  well-marked  lesion.  A  forcible  cardiac  impulse  associated  with 
a  weak  radial  pulse  bespeaks  structural  disease.  The  intensity  of  a  mur- 
mur is  not  an  index  of  the  severity  of  the  lesion,  often  quite  to  the  con- 
trary. Thus  in  failing  compensation  the  murmurs  become  fainter  and 
may  entirely  disappear,  while  the  area  of  cardiac  dulness  increases;  the 
apex  beat  becomes  weaker  and  more  diffuse,  although  sometimes  more 
readily  visible.  Epigastric  pulsation  as  well  as  that  over  the  upper  pre- 
cordium  becomes  more  intense,  and  accentuation  of  the  pulmonic  second 
sound  disappears.  It  is  frequently  impossible  to  make  an  accurate  diag- 
nosis of  the  valvular  lesions  during  broken  compensation. 

The  history  of  an  antecedent  attack  of  rheumatic  fever,  chorea  or 
tonsillitis  is  evidence  in  favor  of  an  organic  lesion,  especially  in  case  of 
the  mitral  valve ;  while  the  history  of  syphilitic  infection  or  the  presence 


HEART   MURMURS  255 

of  a  positive  Wassermann  reaction  more  or  less  definitely  settles  the  origin 
of  a  diastolic  aortic  murmur.  The  presence  of  marked  anemia  should 
make  one  very  chary  of  declaring  a  murmur  to  be  due  to  valvular  disease. 

It  is  to  be  remembered  that  aortic  and  pulmonary  stenosis  are  rare 
lesions,  whereas  systolic  murmurs  over  these  areas  are  very  common. 
At  the  aortic  area  systolic  murmurs  are  usually  due  to  a  mere  roughening 
or  stiffening  of  the  valves  or  to  a  slight  aortic  dilatation.  At  the  pul- 
monary area  systolic  murmurs  may  result  from  the  most  trivial  causes, 
such  as  pressure  of  the  lung,  traction  of  pleural  adhesions,  dilatation  of 
the  artery.  Pulmonary  stenosis  is  practically  always  a  congenital 
lesion,  associated  with  marked  cyanosis,  clubbed  fingers,  right-sided 
hypertrophy,  congestion  of  the  lungs,  a  weak  second  sound  and  thrills. 
Without  some  of  these  findings  a  diagnosis  of  pulmonary  stenosis  should 
never  be  made. 

A  diagnosis  of  tricuspid  insufficiency  cannot  be  made  on  the  presence 
of  a  murmur  alone.  A  positive  venous  pulse,  pulmonary  congestion  or 
hepatic  enlargement,  edema,  ascites,  a  pulsating  liver,  cough,  dyspnea, 
if  not  orthopnea — -at  least  some  of  these  symptoms  must  exist  before  the 
diagnosis  of  tricuspid  insufficiency  is  justified. 

The  presystolic  murmur  of  mitral  stenosis  is  generally  characteristic 
and  readily  recognized  owing  to  its  rumbling  quality  and  to  the  mitral 
pulse.  It  can  be  confused  only  with  a  Flint  murmur  or  with  the  murmur 
of  tricuspid  stenosis.  The  former  is  usually  easily  identified  by  means 
of  the  blood-pressure  picture,  the  marked  left  ventricular  hypertrophy 
and  the  pulsatory  phenomena.  Tricuspid  stenosis  is  a  rare  lesion,  which 
when  encountered  is  generally  associated  with  mitral  stenosis.  But 
few  cases  have  been  correctly  diagnosticated  during  life.  For  obvious 
reasons  they  are  generally  "signed  out"  as  mitral  stenosis.  The  pres- 
ence of  an  "a"  wave  in  the  liver  pulse  is  said  to  be  characteristic  of 
tricuspid  stenosis. 


PART  III 

DISEASES  OF    THE  BRONCHI,   LUNGS,    PLEURA,  AND 

DIAPHRAGM 

By  H.  R.  M.  Landis,  A.  B.,  M.  D. 


CHAPTER  XXI 
DISEASES  OF  THE  BRONCHI 

ACUTE  BRONCHITIS 

An  acute  catarrhal  inflammation  of  the  mucous  membrane  of  the 
trachea,  large  and  medium-sized  bronchi.  In  healthy  adults  it  is,  as  a 
rule,  a  harmless  affection,  but  in  the  very  young  and  very  old  it  is  often 
a  serious  matter.  In  the  latter  age  periods  the  inflammation  shows  a 
decided  tendency  to  extend  downward  into  the  fine  bronchi,  leading 
eventually  to  a  capillary  bronchitis,  or,  as  it  is  preferably  called,  a 
broncho-pneumonia. 

Etiology. — As  met  with  under  ordinary  conditions,  acute  bronchitis 
is  of  itself  of  relatively  little  importance,  and  except  under  the  condi- 
tions above  mentioned,  it  is  rarely  serious.  It  should  be  kept  in  mind, 
however  that  it  is  very  commonly  associated  with  the  acute  infections, 
particularly,  typhoid  fever  and  malaria,  even  from  the  beginning  of 
these  fevers.  Acute  bronchitis  is  so  universally  associated  with 
measles  that  it  should  be  considered  a  symptom  rather  than  a  compli- 
cation. Of  still  greater  importance  is  the  knowledge  that  tuber- 
culosis often  begins  acutely,  and  may  for  a  few  weeks  resemble  an 
attack  of  acute  bronchitis.  Two  facts  should  be  borne  in  mind,  first 
that  acute  bronchitis  runs  its  course  in  about  three  weeks,  and  secondly 
that  it  is  a  bilateral  affection,  while  a  beginning  tuberculosis  is  unilateral 
and  almost  invariably  located  at  the  summit  of  one  or  the  other  lung. 
It  cannot  be  too  strongly  emphasized  that  a  cough  which,  without  com- 
plications, has  persisted  for  six  weeks  or  more  should  be  carefully  inves- 
tigated; the  majority  of  such  cases  will  be  found  to  be  tuberculous. 

It  is  worth  noting  that  individuals  with  tuberculosis  not  infrequently 
give  a  history  of  being  subject  to  repeated  colds. 

Acute  bronchitis  is  especially  prevalent  in  the  changeable  weather 
encountered  in  the  spring  and  late  autumn.  In  some  instances  it  is  the 
result  of  becoming  chilled,  in  others  it  follows  an -ordinary  coryza,  the 
latter  being  in  many  instances  an  acute  infection  transferred  from  person 
to  person.  Individuals  who  are  habitually  closely  confined,  or  who  com- 
monly visit  crowded  places  of  amusement,  or  use  public  conveyances 
17  257 


258      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

are  especially  prone  to  "acute  colds."  On  the  other  hand,  those  who  live 
an  outdoor  life  and  are  subjected  to  all  sorts  of  inclement  weather  are 
comparatively  free  from  these  disorders.  The  contagiousness  of  acute 
colds  was  noted  by  Benjamin  Franklin,  a  century  and  a  half  ago. 

The  bacteriological  findings  in  cases  of  acute  catarrhal  bronchitis  are 
varied.  Occasionally  some  one  organism  predominates  or  even  occurs 
alone,  but  this  is  rare.  Among  the  organisms  encountered  may  be  men- 
tioned the  micrococcus  catarrhalis,  influenza  bacillus,  streptococcus  and 
pneumococcus. 

An  attack  of  acute  bronchitis  may  be  precipitated  by  the  inhalation 
of  dust  or  chemical  irritants,  such  as  ether,  chlorine  gas,  ammonia,  etc. 

Morbid  Anatomy. — Acute  bronchitis  is  practically  always  a  bilateral 
affection  although  the  distribution  of  the  inflammatory  process  is  not 
uniform.  As  a  rule,  certain  portions  of  the  bronchial  tree  are  more  affected 
than  others.  Not  only  are  the  bronchi  affected  but  in  most  instances  the 
trachea  and  larynx  as  well;  indeed  in  some  instances  the  process  may  be 
limited  to  the  larynx,  trachea  and  main  branches  of  the  bronchial  tree 
(see  Fig.  219).  When  the  infection  manifests  itself  principally  in  the 
smaller  tubes  these  are  apt  to  be  small  areas  of  broncho-pneumonia. 
The  latter  may  or  may  not  be  sufficiently  marked  to  be  recognized 
clinically. 

In  simple  catarrhal  bronchitis  the  mucous  membrane  is  reddened  and 
swollen.  It  is  covered  with  a  sticky  exudate  which  is  greyish  in  color 
and  mucoid  in  character.  In  the  later  stages  the  exudate  often  becomes 
mucopurulent  or  purulent. 

Symptoms. — The  onset  is  frequently  with  coryza,  which  as  it  extends 
downward,  successively  causes  some  irritation  of  the  pharynx,  at  times 
hoarseness,  often  marked  in  character,  and  finally  symptoms  indicating 
involvement  of  the  tracheal  and  bronchial  mucous  membranes,  namely, 
a  sense  of  oppression  in  the  chest,  substernal  soreness  and  cough.  The 
latter  is  dry  at  first  and  often  occurs  in  paroxysms  which  cause  marked 
pain  beneath  the  sternum  and  lower  part  of  the  chest.  Fig.  219  illus- 
trates very  clearly  why  this  should  be  so.  The  expectoration  is  at  first 
scanty,  viscid  and  difficult  to  raise.  After  four  or  five  days  the  cough 
tends  to  become  looser,  and  the  sputum  becomes,  first  mucopurulent, 
later  purulent,  and  is  apt  to  be  profuse. 

Slight  fever,  which  may  range  from  100°  to  102°F.  or  higher,  occurs  in 
the  severer  cases.  The  ordinary  case  is  not  febrile  for  more  than  a  week 
or  so.  Later  than  this  the  temperature  becomes  a  valuable  sign  in  dis- 
tinguishing the  condition  from  tuberculosis.  Most  individuals  experience 
a  sense  of  oppression  and  languor.  Pain  in  the  back  and  bones,  not 
unlike  those  encountered  in  grippe,  also  occurs  with  varying  intensity. 

Physical  Signs. — Unless  the  smaller  tubes  are  involved,  as  in  the  aged 
or  very  young,  there  is  no  increase  in  the  respiratoiy  rate.  Aside  from 
the  evidences  indicative  of  an  acute  febrile  state,  inspection  is  negative. 
Percussion  shows  no  changes.  On  palpation  there  may  be  noted  rhonchal 
fremitus. 

The  physical  signs  are  almost  entirely  auscultatory  in  character.  At 
first  the  rales  are  sibilant  in  character,  are  heard  over  both  sides  of  the 
chest,  and  are  very  changeable,  appearing  and  disappearing,  especially 
after  cough.  Later  as  the  cough  loosens  the  rales  have  a  moist  sound  and 
a   bubbling   quality.     While   the   almost   universal  rule  is   that   acute 


Fig.  219. — Intense  acute  bronchitis  due  to  influenza  bacillus.  Upper  lobe  shows 
cavity  at  apex,  great  thickening  of  pleura.  Adhesions  between  lobes.  (Jefferson  Medical 
College  Museum.) 


DISEASES    OF   THE   BRONCHI  259 

bronchitis  is  a  bilateral  affection,  it  occasionally  happens  that  the  physical 
signs  are  confined  to  one  side.  It  is  needless  to  say,  however,  that  such 
cases  are  unusual  and  that  such  a  condition  is  strongly  suggestive  of 
tuberculosis.  Until  the  latter  can  be  ruled  out  positively,  a  diagnosis  of 
acute  bronchitis  is  indefensible. 

Still  another  variation,  and  one  that  is  relatively  common,  is  for  the 
inflammation  to  be  confined  to  the  trachea  alone.  In  these  cases  all  of 
the  symptoms  of  acute  bronchitis  are  present  with  an  absence  of  any 
physical  signs  in  the  chest. 

A  diagnostic  error  is  sometimes  committed,  owing  to  the  fact  that  a 
true  acute  bronchitis  occurs  in  association  with  an  incipient  tuberculosis, 
the  more  serious  affection  thus  becoming  masked.  Even  in  those  cases 
where,  from  the  symptoms,  one  may  suspect  tuberculosis,  the  latter  is 
difficult  to  demonstrate  until  the  bronchitis  has  cleared  up.  After  the 
symptoms,  and  especially,  the  physical  signs,  of  acute  bronchitis  have 
disappeared  the  tuberculous  lesion  can  be  detected. 

Diagnosis. — The  chief  features  of  acute  catarrhal  bronchitis  are 
coryza,  some  irritation  in  the  throat,  substernal  soreness,  cough  and  ex- 
pectoration. For  a  few  days  there  is  usually  a  slight  elevation  of  the 
temperature.  If  the  process  is  limited  to  the  trachea  and  large  tubes 
there  will  be  no  physical  signs;  if  the  medium-sized  bronchi  are  involved, 
rales  will  be  heard  over  both  lungs.  Of  itself  acute  bronchitis  is  a  trivial 
affection.  It  is  always  worthy  of  consideration,  however,  as  it  is  often 
the  forerunner  of  more  serious  trouble.  In  children  and  in  those  of 
advanced  years  the  possibility  of  the  inflammatory  process  extending  to 
the  finer  bronchi  and  air  cells  must  always  be  borne  in  mind. 

In  children  catarrhal  inflammation  of  the  conjunctiva  and  nasal 
mucous  membrane  associated  with  cough  and  expectoration,  may  be 
the  prodromal  symptoms  of  measles.  The  mucous  membrane  of  the 
mouth  should  be  examined  for  the  presence  of  Koplik's  spots.  The 
symptoms  in  the  early  stage  of  whooping-cough  are,  as  a  rule,  those  of 
an  acute  cold,  the  characteristic  whoop  not  appearing  until  later.  In 
the  presence  of  an  epidemic  of  whooping  cough  an  acute  "cold"  should  be 
looked  upon  as  possibly  being  the  prodromal  stage  of  pertussis. 

Not  infrequently  patients  who  develop  lobar  pneumonia  will  give  a 
history  of  having  had  a  "bad  cold"  for  some  days  before  the  onset  of  the 
pneumonia.  Acute  bronchitis  is  so  constantly  present  in  cases  of 
typhoid  fever  as  to  constitute  a  symptom  of  the  disease.  It  may  occur 
early  in  the  attack  of  typhoid  fever.  In  an  individual  suffering  from  what 
appears  to  be  an  attack  of  acute  bronchitis  and  in  whom  the  fever  persists 
and  prostration  is  marked,  typhoid  fever  should  be  thought  of. 

The  differentiation  between  acute  bronchitis  and  early  tuberculosis 
is  considered  on  page  315. 

CHRONIC  BRONCHITIS 

Etiology. — As  a  primary  affection,  chronic  bronchitis  is  encountered 
much  less  frequently  than  is  usually  thought,  and  while  it  is  commonly 
taught  that  repeated  attacks  of  acute  bronchitis  .may  develop  into  the 
chronic  form  of  the  disease,  such  is  rarely  the  case.  Indeed  there  are 
some  who  refuse  to  recognize  the  existence  of  a  primary  chronic  bron- 
chitis under  any  circumstances.     It  is  certain  that  many  cases  so  dcsig- 


260      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

nated  are  in  reality  instances  in  which  a  much  more  serious  affection  is 
present,  the  bronchitis  being  only  a  secondary  manifestation  There  is 
one  class  of  cases,  however,  in  which  chronic  bronchitis  is  very  frequently 
a  primary  affection,  namely,  those  in  which  there  has  been  a  prolonged 
exposure  to  dust,  such  as  is  seen  in  millers,  stone  cutters,  coal  miners,  etc. 
In  these  cases  the  constant  irritation  produced  by  the  dust  particles, 
which  at  first  produces  a  mild  acute  inflammatory  condition  of  the 
bronchial  mucous  membrane,  finally  brings  about  a  chronic  condition. 
It  is  worth  bearing  in  mind,  however,  that  the  morbidity  from  tuber- 
culosis is  very  high  among  such  workers,  and  care  must  be  exercised 
not  to  mistake  a  latent  tuberculosis  for  chronic  bronchitis. 

Chronic  bronchitis  is  rarely  encountered  in  the  young;  on  the  other 
hand,  it  is  very  frequent  among  those  past  the  middle  period  of  life. 
The  winter  cough  so  frequently  encountered  in  those  of  advanced  years 
is  usually  one  of  the  indications  of  a  faulty  circulation,  a  chronic  renal 
lesion  or  some  chronic  pulmonary  condition  such  as  asthma  or  emphy- 
sema. Indeed,  it  is  in  association  with  these  latter  conditions  that 
chronic  bronchitis  is  most  frequently  met  with.  In  such  individuals 
climatic  changes  have  an  important  bearing;  they  are  extremely  suscepti- 
ble to  sudden  changes  in  the  weather.  In  the  warm  summer  months 
they  are  almost  entirely  free  from  their  pulmonary  symptoms,  and  resi- 
dence in  a  warm  climate  during  the  winter  months  also  assures  them  of 
freedom  from  their  symptoms. 

Gout,  chronic  alcoholism,  certain  skin  lesions  and  obesity  also  are  not 
uncommonly  accompanied  with  chronic  bronchitis.  Rarely  a  tumor  or 
aneurism  of  the  aorta,  through  pressure  on  the  bronchi,  may  bring  about 
a  catarrhal  inflammation  of  the  bronchial  mucous  membrane,  and  finally 
a  chronic  bronchitis.  It  is  thus  seen  that  in  the  vast  majority  of  instances 
the  condition  is  secondary  to  some  other  affection,  and  until  disease  of  the 
heart,  kidney  or  other  pulmonary  lesions  are  excluded  a  diagnosis  of 
chronic  bronchitis  alone  is  untenable. 

Morbid  Anatomy. — The  condition  is  characterized  by  a  venous  hy- 
peremia and  swelling  of  the  bronchial  mucous  membrane  with  increased 
secretion  of  mucus,  and  the  exudation  of  serum  and  pus  cells.  As  the 
disease  progresses  the  mucous  membrane  may  hypertrophy  in  places, 
and  in  others  become  atrophied,  so  that  the  longitudinal  bands  of  elastic 
tissue  are  readily  'seen.  The  membrane  is  also  frequently  denuded  of 
its  epithelium  and  the  glandular  tissues  atrophied.  Of  the  end  results, 
cylindrical  dilatation  of  the  medium  and  smaller  bronchi  is  frequent, 
while  some  degree  of  emphysema  is  constantly  met  with. 

Symptoms. — The  chief  manifestations  are  as  follows:  Shortness  of 
breath  on  the  slightest  exertion,  which  is  sometimes  accompanied  by  a 
fit  of  coughing,  with  or  without  expectoration.  These  symptoms  espe- 
cially the  shortness  of  breath  are  commonly  due  to  the  associated  emphy- 
sema; in  some  cases  cardiac  weakness  is  the  exciting  factor.  The  cough, 
as  already  stated,  is  variable,  being  much  influenced  by  the  weather 
conditions.  In  the  summer  it  is  very  slight,  or  even  disappears  alto- 
gether. Even  in  the  winter  it  is  not  apt  to  be  constant,  and  during  this 
season  may  occur  only  in  the  morning,  or  there  may  be  a  paroxj^sm  at 
night.  The  expectoration  also  varies  greatly  in  different  cases;  in  some 
it  is  entirely  absent.  As  a  rule,  however,  it  is  rather  abundant  and  muco- 
purulent in  character. 


DISEASES    OF   THE   BRONCHI  261 

There  is  no  pain  nor  fever,  and  rarely  any  marked  deterioration  of 
health.  The  most  serious  feature  of  the  disease  is  the  fact  that  it  prac- 
tically always  results  in  emphysema,  and  in  some  instances,  leads  to  a 
severe  grade  of  bronchiectasis. 

Physical  Signs. — Chronic  bronchitis,  primary  in  character,  like  the 
acute  form  has  few  physical  signs,  and  those  are  entirely  auscultatory. 
Inasmuch,  however,  as  the  disease  is  nearly  always  associated  with  some 
emphysema,  and  occasionally  with  well-marked  dilatation  of  the  bronchi, 
the  physical  signs  vary  in  individual  cases. 

In  the  ordinary  case  with  slight  emphysematous  changes,  the  follow- 
ing points  may  be  noted: 

Inspection. — Barrel-shaped  chest  with  little  or  no  lateral  expansion, 
the  chest  moving  up  and  down.  The  apex  beat  of  the  heart  is  usually 
not  seen  because  of  the  distended  lung.  These  signs  may  be  very  marked, 
or  hardly  evident,  depending  entirely  on  the  amount  of  emphysema 
present. 

Palpation. — Palpation  confirms  the  character  of  the  expansion. 
Vocal  fremitus  is  normal  or  slightly  diminished.  A  rhonchal  fremitus 
may  be  detected  at  different  points. 

Percussion. — The  percussion  note  is  normal  or  hyperresonant  in  ac- 
cordance with  the  amount  of  emphysema  present.  It  may  also  have  a 
tympanitic  quality  at  the  bases  as  the  result  of  pulmonary  relaxation, 
or  if  the  secretion  is  profuse,  the  note  may  be  slightly  impaired  in  the 
same  situation. 

Auscultation. — The  auscultatory  signs  will  vary  in  accordance  with 
the  amount  of  secretion  present.  Thus  in  the  summer  months  when  the 
patient  is  free  from  cough,  the  lungs  may  reveal  no  adventitious  sounds 
whatever,  and  aside  from  a  slight  diminution  of  the  intensity  of  the  respira- 
tory murmur  and  prolonged  expiration  show  no  marked  deviation  from 
the  normal.  During  the  active  stage,  however,  the  lungs  are  usually 
filled  with  mixed  rales,  both  large  and  small,  and  at  one  time  or  another 
they  are  heard  everywhere  throughout  both  lungs.  At  the  bases  of  the 
lungs  the  rales  are  quite  apt  to  be  of  the  small  moist  variety.  At  times 
the  rales  are  so  numerous  and  loud  as  to  entirely  obscure  the  respiratory 
murmur.     Vocal  fremitus  may  be  normal  or  diminished  in  intensity. 

Diagnosis. — The  recognition  of  chronic  bronchitis  is  not  difficult. 
The  important  thing  to  bear  in  mind  is  that  it  is  almost  invariably  a  sec- 
ondary condition  and  is  only  too  often  one  of  the  manifestations  of  a 
much  more  serious  affection. 

FIBRINOUS  BRONCHITIS 

The  disease  is  also  referred  to  as  plastic,  croupous  or  pseudo-mem- 
branous bronchitis  and  bronchial  croup.  The  essential  feature  of  this 
form  of  bronchitis  is  the  formation  in  the  bronchial  tubes  of  fibrinous 
casts,  which  are  expelled  after  a  paroxysm  of  dyspnea  and  cough.  It 
is  a  rare  affection  and  although  known  to  Galen  and  other  ancient  authors 
the  number  of  cases  recorded  in  the  literature  is  not  much  over  two 
hundred.  The  disease  may  occur  either  as  an  acute  or  a  chronic  mani- 
festation; the  latter  is  by  far  the  most  frequent.  . 

Bronchial  casts  may  be  formed  secondarily  to  diphtheria  in  the 
pharynx  or  larynx  or  to  croupous  pneumonia.  Casts  occurring  in 
association  with  these  two  diseases  will  not  be  considered  here. 


262      DISEASES   OF  THE  BRONCHI,   LUNGS,   PLEURA,    AXD   DIAPHRAGM 

Etiology. — The  cause  of  fibrinous  bronchitis  is  as  yet  wholly  unknown 
and  there  is  no  evidence  to  show  that  it  is  in  any  way  dependent  on  a 
bacterial  infection.  The  disease  occurs  most  frequently  between  the 
ages  of  ten  and  thirty.  Males  are  affected  about  twice  as  frequently  as 
females.  In  common  with  other  forms  of  bronchitis  this  form  of  the 
disease  occurs  more  frequently  in  the  colder  months  of  the  year. 

The  immediate  exciting  causes  are  probably,  in  great  measure,  the 
same.  In  one  instance  a  simple  bronchitis  develops;  in  the  other  a 
fibrinous  exudation  is  later  superadded. 

Fibrinous  bronchitis  has  been  described  as  occurring  in  association 
with  a  variety  of  conditions  but  in  most  instances  the  connection  is  to  be 
regarded  as  no  more  than  a  coincidence.  It  has  been  noted  in  the  course 
of  the  acute  infections  such  as  measles,  scarlet  fever,  erysipelas,  typhoid 
fever,  influenza,  etc.  The  inhalation  of  irritant  fumes  and  gases  such  as 
steam,  smoke  and  ammonia,  has  at  times  been  followed  by  the  expulsion 
of  fibrinous  casts.  Among  other  conditions  reported  may  be  mentioned 
asthma,  pulmonary  edema  following  thoracentesis,  pulmonary  actino- 
mycosis and  aspergillosis  and  various  skin  diseases. 

"  The  largest  number  of  instances  have  been  met  with  in  individuals 
affected  with  heart  disease  and  pulmonary  tuberculosis.  In  regard  to 
tuberculosis  the  frequency  of  the  association  varies  tremendously  among 
different  observers.  West1  refers  to  the  association  of  fibrinous  bronchitis 
and  tuberculosis  in  7  out  of  51  cases.  Lehmann-Model2  found  tubercu- 
losis at  autopsy  in  3  of  6  cases  observed  by  him  and  refers  to  26  autopsies 
in  the  literature  in  which  tuberculosis  was  found  in  10.  I  recall  no  in- 
stance of  bronchial  casts  occurring  among  the  ward  patients  in  the  Phipps 
Institute  over  a  period  of  thirteen  years  nor  have  such  casts  ever  been 
found  in  any  of  the  662  autopsies  on  tuberculous  individuals.  Walshe3 
also  emphasizes  the  fact  that  he  had  never  seen  the  true  disease  either  in 
life  or  in  death  in  an  actively  phthisical  person.  It  is  probably  fair  to 
assume  that  pulmonary  tuberculosis  plays  no  part  in  the  formation  of  the 
casts  and  that  the  association  of  the  two  conditions  is  a  mere  coincidence. 
The  same  may  be  said  of  the  association  with  heart  disease. 

In  a  certain  number  of  instances  the  disease  occurs  in  robust,  healthy 
individuals  in  whom  there  is  no  apparent,  causative  factor. 

Morbid  Anatomy. — The  bronchi  involved  usually  represent  a  circum- 
scribed area  but  occasionally  the  disease  occurs  in  a  diffuse  form.  While 
any  part  of  the  bronchial  tree  may  be  involved  the  bronchi  of  the  lower 
lobes  are  most  frequently  affected"  (West).  The  process  as  a  rule,  com- 
mences in  the  medium-sized  bronchi  and  extends  downward.  There  is 
little  tendency  to  spread  upward.  While  it  is  known  that  the  diph- 
theria bacillus  by  extension  downward,  may  produce  a  fibrinous  cast  in 
the  trachea  and  large  bronchi  and  that  the  pneumococcus  may  lead  to 
the  formation  of  casts  in  the  small  bronchi  during  an  attack  of  pneumonia, 
there  is  no  evidence  to  show  that  fibrinous  casts  occurring  either  idio- 
pathically  or  in  association  with  other  conditions,  are  bacterial  in  origin. 
As  to  the  bronchi  themselves  there  is  no  constantly  associated  lesion. 
Occasionally  a  case  has  been  reported  in  which  at  the  site  of  the  cast, 
there  has  been  a  caseous  infiltration,  an  ulcer  or  desquamation  of  the 

1  "Diseases  of  the  Respiratory  Organs.'" 

2  Inaugural  Dissertation,  Freiburg,  1890. 

3  "Diseases  of  the  Lungs,"  4th  ed.,  1871. 


DISEASES    OF    THE    BRONCHI 


263 


epithelium.  In  none  of  these  cases,  however,  is  it  clear  that  the  change 
in  the  bronchi  bore  any  causal  relation  to  the  formation  of  the  cast.  In 
the  chronic  form  of  the  disease,  emphysema  of  the  lungs  sometimes 
develops. 

The  casts  are  pearly  gray  or  white  in  color  and  of  fairly  firm  consist- 
ency. They  vary  in  length  from  fragments  %  inch  long  up  to  complete 
casts  of  6  or  7  inches,  with  branches  corresponding  to  the  divisions  of  the 
bronchi  from  which  they  have  been  expelled  (Fig.  220).  The  casts  from 
the  larger  bronchi  are  hollow  and  present  a  laminated  appearance  as  the 
result  of  successive  deposits  of  fibrin  or  mucus.  The  smaller  casts  are 
solid  and  often  terminate  in  spirals. 


Fig.  220. — Fibrinous  bronchitis  cast  expectorated;  three-fourths  natural  size. 
Bettmann,  in  American  Journal  of  the  Medical  Sciences.) 


(Milton 


Bronchial  casts  are  usually  composed  chiefly  of  fibrin,  but  in  some 
instances  the  main  constituent  is  mucus  and  in  others  the  fibrin  and 
mucus  occur  together  in  varying  proportions.  At  times  the  cast  is 
streaked  with  blood.  The  number  expelled  varies  from  one  every  day 
or  so  to  a  large  number  daily.  They  may  be  coughed  up  as  a  lump  or 
pellet  or  may  be  surrounded  by  sputum.  The  discovery  of  the  cast  is 
often  accidental.  The  patient  may  be  led  to  examine  the  pellet,  as  in 
a  case  recently  observed,  or  the  true  nature  of  the  small  lumps  may  be 
revealed  in  the  course  of  the  examination  of  the  sputum.  The  sputum 
may  be  scanty  or  very  profuse.  In  addition  t©  the  presence  of  casts 
the  sputum  may  contain  Charcot-Leyden  crystals,  Curschmann's  spirals 
and  eosinophilic  cells,  indicating  a  condition  of  the  mucous  membrane 
similar  to  that  in  asthma  (McPhedran). 


264      DISEASES   OF   THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

Symptoms. — Two  forms  of  the  disease  are  recognized,  the  acute  and 
the  chronic.  The  acute  form  which  is  rare,  may  begin  abruptly  with  a 
chill,  fever,  cough,  pain  in  the  chest  and  dyspnea.  It  is  more  apt,  how- 
ever, to  be  associated  with  one  of  the  acute  infections,  in  which  case, 
after  a  preliminary  bronchitis  the  paroxysms  of  coughing  become  more 
and  more  severe  and  the  dyspnea  increases.  The  fibrinous  casts,  the 
presence  of  which  alone  make  the  diagnosis  possible,  may  be  coughed  up 
at  once  or  after  the  existence  of  some  days  of  what  seems  to  be  a  simple 
bronchitis. 

The  duration  of  the  acute  cases  is  from  a  few  days  to  several  weeks. 
In  the  favorable  cases  the  fever  declines  by  lysis,  the  cough  and  dyspnea 
diminish,  the  expectoration  of  casts  ceases  and  there  is  complete  and 
permanent  recovery.  In  severe  cases  death  often  occurs  with  all  the 
symptoms  of  suffocation. 

Rarely  the  acute  form  may  become  chronic  but  this  is  very  unusual. 
The  chronic  variety  is  often  preceded  by  the  ordinary  chronic  form  of 
bronchitis  although  in  some  instances  the  disease  may  assume  the  fibrin- 
ous type  from  the  outset.  The  attacks  tend  to  recur  at  certain  definite 
intervals  for  months  or  years.  In  some  instances  the  size  of  the  casts  is 
identical  in  each  attack  and  this  fact  in  association  with  the  location  of 
the  physical  signs,  points  to  the  involvement  of  the  same  portion  of  the 
bronchial  tree.  During  the  attack  the  cough  assumes  a  paroxysmal 
character  and  dyspnea  is  marked. 

Hemoptysis  has  been  noted  in  a  number  of  cases.  The  amount  of 
blood  expectorated  is  usually  small  and  may  consist  of  nothing  more  than 
some  blood  streaks  on  the  cast.  Epistaxis,  diarrhea  and  albuminuria 
have  been  noted  during  an  attack.  In  the  chronic  form  there  is 
rarely  any  fever  or  any  other  evidence  of  constitutional  disturbance 
and  the  general  nutrition  is  well  maintained.  Emphysema  often 
develops. 

In  the  chronic  form  the  attack,  consisting  of  paroxysms  of  dyspnea 
and  coughing  followed  by  the  expulsion  of  a  cast,  may  last  from  a  few 
clays  to  weeks  or  even  months.  The  separate  paroxysm  is  usually  short 
although  it  may  be  preceded  by  some  hours  of  coughing.  The  attacks 
vary  greatly  in  duration  even  in  the  same  patient. 

Once  the  chronic  form  develops  the  patient  is  usually  liable  to  attacks 
the  remainder  of  life.  The  disease  has  been  noted  to  recur  over  a  period 
of  twenty-five  years.  The  interval  between  the  attacks  varies.  In 
some  instances  the  attacks  recur  regularly  at  certain  times,  as  for  instance 
at  the  menstrual  periods ;  in  others  it  comes  irregularly  and  there  may  be 
an  interval  of  years  in  which  the  patient  is  free  from  the  disease. 

Physical  Signs. — The  physical  signs  do  not  give  definite  information. 
If  but  a  small  area  is  involved  they  may  be  entirely  normal.  In  many 
instances  the  physical  findings  are  those  of  acute  or  chronic  bronchitis. 
If  a  sufficiently  large  area  is  involved  there  may  be  deficient  expansion 
on  the  affected  side,  a  weakened  or  absent  respirator}-  murmur,  dulness 
and  the  presence  of  rales  both  large  and  small.  These  atelectatic  areas 
disappear  with  the  expulsion  of  the  cast. 

The  abnormal  physical  signs  are  commonly  found  at  the  bases  of 
the  lungs  and  usually  on  one  side  only.  The  only  physical  sign  peculiar 
to  fibrinous  bronchitis  is  a  curious  flapping  sound  beginning  in  the  middle 
of  inspiration  and  continuing  to  the  end.     It  is  apparently  produced 


DISEASES    OF    THE   BRONCHI  265 

by  the  presence  of  partially  separated  casts.  Its  value  is  limited, 
however,  as  it  is  present  in  but  a  small  minority  of  cases. 

Diagnosis. — A  diagnosis  of  fibrinous  bronchitis  is  possible  only  by 
the  detection  of  the  casts.  These  may  be  so  surrounded  by  the  sputum 
as  to  escape  notice.  As  already  stated  they  may  be  accidentally  dis- 
covered by  the  patient  or  they  may  be  detected  in  a  routine  sputum 
examination.  The  condition  is  to  be  suspected  in  patients  who  give  a 
history  of  recurring  attacks  of  paroxysmal  cough  and  dyspnea.  In 
individuals  seen  during  the  first  attack,  however,  the  finding  of  a  bronchial 
cast  is  the  only  criterion. 

The  following  case  is  an  excellent  example  of  the  so-called  idiopathic 
fibrinous  bronchitis:  The  patient  was  a  robust,  healthy  male,  aged 
47,  referred  to  me  because  of  suspected  tuberculosis.  The  family  history 
was  negative  and  he  had  never  had  any  illness.  Four  weeks  prior  to 
his  coming  under  my  observation  he  had  caught  "cold."  The  trouble 
started  as  a  coryza  and  in  a  few  days  he  developed  a  severe  paroxysmal 
cough  and  some  dyspnea.  For  the  first  two  weeks  the  sputum,  which 
was  moderate  in  amount,  was  thick  and  whitish  in  color,  later  it  had  a 
greenish  tinge.  On  one  occasion  after  a  paroxysm  of  coughing  he  spat 
into  his  handkerchief  a  small  hard  pellet  which  on  examination  proved 
to  be  a  cast  from  one  of  the  medium-sized  bronchi.  There  was  a  slight 
elevation  of  temperature  during  the  attack.  The  sputum  was  negative 
for  tubercle  bacilli  but  contained  both  pneumococci  and  streptococci. 
With  the  exception  of  one  day  spent  in  bed  he  attended  to  his  professional 
work,  although  with  some  effort.  His  appetite  was  good  and  he  had 
lost  no  weight. 

On  physical  examination  there  was  deficient  expansion  at  the  right 
base,  impairment  of  the  percussion  note,  suppressed  breath  sounds,  both 
large  and  small  rales  and  in  addition  a  "napping  sound"  heard  at  the 
end  of  inspiration.  The  patient  was  sent  to  the  seashore  and  when  seen 
two  weeks  later  there  was  nothing  abnormal  to  be  noted  over  the  area 
previously  affected. 

The  localization  of  the  physical  signs,  usually  at  the  base  of  one  lung, 
should  serve  to  differentiate  the  condition  from  simple  bronchitis.  The 
lodgment  of  a  foreign  body  in  one  of  the  medium-sized  bronchi  is  apt  to 
give  rise  to  localized  physical  signs  over  the  lower  lobe  of  one  lung  but 
in  such  cases  the  evidences  of  pulmonary  mischief  are  permanent  and 
in  addition  casts  are  not  expelled  in  the  sputum.  Owing  to  the  par- 
oxysmal character  of  the  attacks  and  the  dyspnea  fibrinous  bronchitis 
may  be  mistaken  for  asthma.  In  the  latter  condition  the  physical  signs 
are  bilateral  and  the  respiratory  difficulty  is  expiratory  in  nature.  The 
finding  of  bronchial  casts  is  the  deciding  factor  in  all  cases. 

BRONCHIOLITIS  FIBROSA  OBLITERANS 

Our  knowledge  of  this  condition  is  of  recent  origin.  Occlusion  of  the 
finer  bronchi,  independent  of  other  marked  lesions  of  the  lung,  was  first 
described  by  Lange1  in  1901.  The  following  year  Frankcl2  reported  the 
first  case  in  which  the  diagnosis  was  made  during  life  and  a  few  years 
later  he3  reported  three  additional  cases. 

1  Deut.  Arch.  f.  kl.  Med.,  Bd.  lxx,  p.  342. 

2  Ibid,  1902,  lxxii,  p.  484. 

3  Berliner,  kl.  Woch.,  1909,  xlvi,  6. 


266      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

Etiology. — In  one  of  Frankel's  cases  the  condition  followed  the 
inhalation  of  nitrogen  tetroxide  fumes,  in  another  the  inhalation  of  lime 
and  other  dust;  in  his  remaining  two  cases  the  cause  was  not  definitely 
established.  Edens1  observed  a  case  resulting  from  the  inhalation  of  the 
fumes  from  a  mixture  of  hydrochloric  and  nitric  acid.  In  addition  to 
these  cases  the  causation  of  which  is  reasonably  clear,  similar  pathological 
changes  have  been  reported  as  having  followed  measles,  whooping  cough, 
syphilis,  uncomplicated  catarrhal  inflammation  of  the  finer  tubes  and 
the  aspiration  of  a  foreign  body.  It  would  seem,  therefore,  that  any 
condition  capable  of  causing  inflammation  of  the  finer  bronchi  and 
bronchioles  may  be  followed  by  occlusion  of  this  portion  of  the  bronchial 
tree.  On  the  other  hand  either  such  an  occurrence  is  rare,  except  in  the 
case  of  irritating  gases,  or  it  is  not  generally  recognized. 

Morbid  Anatomy. — In  the  cases  reported  by  Frankel  and  Edens, 
following  the  inhalation  of  a  toxic  gas,  the  lungs  presented  the  appearance 
usually  seen  after  such  accidents  (see  p.  481).  In  addition  the  cut  sur- 
face snowed  numerous  small  grayish-white  nodules  from  1  to  2  mm.  in 
diameter  which  closely  resembled  miliary  tubercles.  On  examination 
with  a  hand  glass  these  small  nodules  are  seen  to  differ  from  miliary 
tubercles  in  that  they  are  angular  or  stellate  in  form.  Futhermore 
they  are  found,  on  dissection,  to  be  the  terminal  portion  of  the  smaller 
bronchi.  Microscopically  the  finer  bronchi  show  marked  epithelial 
desquamation,  the  cells  often  blocking  the  tube.  In  addition  there  is 
an  ingrowth  of  connective  tissue  which  may  completely  occlude  the 
lumen  or  reduce  it  to  a  small  slit.  The  connective  tissue  apparently 
takes  its  origin  from  the  bronchial  wall.  Connective-tissue  invasion  of 
the  adjacent  alveoli  may  take  place  also. 

Symptoms. — The  dominant  symptoms  are  intense  dyspnea  and 
cyanosis.  If  the  inhalation  of  irritating  vapors  has  occurred  there  may 
be  present  also  cough  and  the  expectoration  of  reddish-brown  sputum. 
The  pulse  is  very  rapid.  The  percussion  note  is  hyperresonant  as  the 
result  of  emphysema  and  on  auscultation  numerous  fine  rales  are  heard. 
In  one  of  Frankel's  cases  the  symptoms  developed  sixteen  days  after  the 
inhalation  of  an  irrespirable  gas;  death  occurred  three  days  later.  In 
Edens'  case  the  symptoms  developed  ten  days  after  the  inhalation  of 
gas,  death  taking  place  on  the  twenty-sixth  day.  It  would  seem  that 
the  appearance  of  the  dyspnea  and  cyanosis  coincide  with  the  subsidence 
of  the  acute  inflammation  and  the  occlusion  of  the  bronchioles  as  the 
result  of  connective  tissue  proliferation. 

Diagnosis. — In  an  individual  who  is  known  to  have  inhaled  a  poison- 
ous gas  and  in  whom  there  is  a  temporary  amelioration  or  subsidence  of 
the  symptoms,  a  diagnosis  of  bronchitis  or  bronchiolitis  obliterans  may 
be  ventured  if  there  develops  severe  dyspnea  and  cyanosis  associated 
with  hyperresonance  and  fine  rales.  If,  however,  the  condition  follows 
measles,  whooping  cough,  or  any  condition  associated  with  a  catarrhal 
inflammation  of  the  finer  bronchi  a  correct  diagnosis  would  be  a  matter 
of  luck.  Acute  miliary  tuberculosis  and  broncho-pneumonia  may  mani- 
fest themselves  in  the  same  way.  In  the  great  majority  of  cases  the 
condition  must  be  looked  upon  as  of  pathological  interest.  It  is  quite 
possible,  however,  that  some  cases  which  have  been  diagnosed  as  miliary 
tuberculosis  of  the  lungs  by  the  X-rays  and  which  subsequently  recovered, 
1  Deut.  Arch.  f.  kl.  Med.,  1905,  lxxx,  598. 


DISEASES    OF   THE   BRONCHI  267 

are  of  this  nature.  Inasmuch  as  the  nodules  present  a  strong  resem- 
blance to  miliary  tubercles  when  the  lung  is  exposed  to  direct  inspection 
it  can  be  readily  understood  how  easily  a  mistake  could  be  made  in  inter- 
preting an  X-ray  plate.  I  have  knowledge  of  one  case  in  which  a  diag- 
nosis of  miliary  tuberculosis  was  made  because  of  the  presence  in  the 
plate  of  numerous  small  nodules  which  were  taken  for  tubercles.  The 
patient  is  alive  and  well  after  an  interval  of  two  years. 

WHOOPING  COUGH   (PERTUSSIS) 

This  disease  is  primarily  a  tracheo-bronchitis  which  is  characterized 
by  a  series  of  violent  spasmodic  coughs  which  end  in  a  long  drawn  inspira- 
tion or  "whoop."  It  is  allied  to  other  forms  of  bronchitis  but  differs  from 
them  in  that  it  has  a  definite  specific  cause,  the  Bordet-Gengou  bacillus, 
and  also  because  of  the  paroxysmal  cough  followed  by  spasm  of  the  glot- 
tis  during  inspiration. 

Whooping  cough  was  at  one  time  looked  upon  as  a  relatively  harm- 
less affection  and  is  still  regarded  as  such  by  many  of  the  laity.  It 
cannot  be  too  strongly  emphasized  that  it  is  a  most  dangerous  disease  in 
young  children.  The  custom  of  deliberately  exposing  children  to  this 
infection  with  the  idea  that  it  is  a  necessary  episode  in  childhood  should 
be  discouraged.  In  recent  years  departments  of  health  have  repeatedly 
warned  people  in  this  regard.  Of  itself  the  disease  is  distressing,  chiefly 
because  of  the  violence  of  the  paroxysms  of  coughing.  Its  danger  lies  in 
the  complications  and  sequels  which  occur  so  frequently,  the  most 
serious  of  which  are  broncho-pneumonia  and  tuberculosis. 

Etiology. — It  is  essentially  a  disease  of  young  children.  The  largest 
proportion  of  cases  occur  between  the  first  and  second  dentition.  It 
may  occur,  however,  in  infants  but  a  few  weeks  old  and  not  infrequently 
it  is  encountered  in  adults.  One  attack  almost  invariably  confers  perma- 
nent immunity.  A  second  attack  occurs  very  rarely.  The  disease 
usually  manifests  itself  in  more  or  less  widespread  epidemics,  particularly 
in  the  winter  and  spring  months.  In  large  communities,  however,  iso- 
lated cases  are  apt  to  be  encountered  at  all  times.  The  disease  appears 
to  be  most  contagious  during  the  first  or  catarrhal  period.  It  has  long- 
been  noted  that  epidemics  of  whooping  cough  and  measles  bear  a  curious 
relation  to  each  other.  The  appearance  of  either  one  of  these  diseases 
is  often  preceded  or  followed  by  the  other.  Less  frequently  the  same 
is  true  of  scarlet  fever. 

The  exciting  cause  of  whooping  cough  is  now  quite  generally  ad- 
mitted to  be  the  minute  bacillus  described  by  Bordet  and  Gengou, 
commonly  known  as  the  Bordet-Gengou  bacillus.  The  proof  seems  to  be 
conclusive.  With  this  organism  Mallory,  Hornor  and  Henderson1  have 
been  able  to  produce  the  characteristic  lesion  of  the  disease  in  young 
animals  and  to  recover  the  bacillus  in  pure  culture.  The  results  obtained 
by  Olmstead  and  Luttinger2  in  a  study  of  the  complement  fixation  test 
inlllcases  of  whooping  cough  or  suspected  whooping  cough  also  support 
the  claim  that  the  Bordet-Gengou  bacillus  is  the  true  etiological  factor. 

Morbid  Anatomy. — The  characteristic  lesion  of  the  disease  is  found 
in  the  trachea  and  bronchi,  especially  the  former.     The  opportunity  of 

1  Jour.  Med.  Res.,  March,  1913. 

2  Arch.  Int.  Med.,  July,  1915. 


268       DISEASES    OF   THE  BROXCHI,    LUNGS,    PLEURA,    AXD    DIAPHRAGM 

studying  the  pathological  changes  in  the  acute  stage  of  the  disease  does 
not  happen  very  frequently  as  death  is  most  apt  to  occur  at  a  later 
period.  In  the  few  cases  studied  by  Mailory  and  Hornor1  the  micro- 
scopic examination  showed  large  numbers  of  minute  bacteria  between 
the  cilia  of  many  of  the  cells  lining  the  trachea.  The  cilia  of  single  cells 
or  large  groups  of  cells  may  be  affected.  The  organisms  usually  reach 
the  base  of  the  cilia  but  may  extend  only  part  way.  They  frequently 
cause  a  lateral  spreading  or  mushrooming  of  the  cilia  covering  a  single 
cell.  In  many  places  the  cilia  are  reduced  to  short  stubs  or  are  entirely 
wanting.  The  action  of  bacteria  appears  to  be  largely  mechanical  leading 
to  interference  with  the  normal  movements  of  the  cilia  by  sticking  them 
together.     In  this  way  the  microorganisms  furnish  a  continual  irritation. 

The  most  serious  of  the  effects  of  whooping  cough  are  to  be  found  in 
the  complications.  A  common  cause  of  death  is  broncho-pneumonia 
winch  is  often  tuberculous  in  character.  Areas  of  atelectasis,  either 
alone  or  in  association  with  broncho-pneumonia,  are  frequently  seen. 
Enlargement  of  the  bronchial  lymph  nodes  is  a  common  result  of  whoop- 
ing cough,  and  in  many  cases  areas  of  caseation  due  to  tuberculosis  are 
present.  The  paroxysms  of  coughing  may  lead  to  over  distention  of  the 
lungs  (emphysema).  Among  the  more  unusual  complications  may  be 
mentioned  an  acute  form  of  bronchiectasis  (bronchiolectasis,  see  page  286) , 
interstitial  and  mediastinal  emphysema  and  pneumothorax,  the  last- 
named  conditions  being  caused  by  the  rupture  of  the  lung. 

Symptoms. — It  is  customary  to  divide  the  clinical  manifestations  of 
whooping  cough  into  three  stages:  (1)  The  prodromal  or  catarrhal; 
(2)  the  paroxysmal  or  spasmodic ;  and  (3)  the  stage  of  gradual  disappear- 
ance of  the  cough  and  spasm.  This  division  is  somewhat  arbitrary  and 
does  not  hold  true  for  all  cases.  In  some  instances  the  disease  may  begin 
with  violent  paroxysms  of  coughing;  in  others  the  characteristic  whoop 
may  be  wanting. 

Between  the  time  of  exposure  and  the  appearance  of  the  first  symp- 
toms there  is  a  variable  incubation  period  of  from  seven  to  ten  days.  In 
the  catarrhal  stage  the  symptoms  are  those  of  an  ordinary  cold.  There 
is  slight  fever,  running  at  the  nose,  injection  of  the  conjunctiva  and  a 
cough.  Even  at  this  time  the  cough  may  be  spasmodic  but,  as  a  rule,  it 
is  such  as  occurs  in  an  attack  of  simple  bronchitis.  There  is  this  distinc- 
tion, however,  that  the  cough  is  somewhat  more  frequent  and  obstinate, 
both  in  children  and  adults,  and  that  the  patient  has  a  more  troublesome 
sensation  of  tickling  in  the  throat  and  inside  the  trachea  (Trousseau). 
The  catarrhal  stage  lasts  from  a  week  to  ten  days. 

The  paroxysmal  stage  dates  from  the  time  of  the  first  ''whoop. "  The 
cough  now  assumes  a  definite  paroxysmal  character.  The  paroxysm 
is  often  preceded  by  pain  beneath  the  sternum  and  a  sensation  of 
tickling  or  pricking  in  the  larynx  and  trachea.  The  coughing  fit 
commences  with  a  noisy  expiration  followed  by  a  series  of  from  fifteen 
to  twenty  forcible,  short  coughs  of  increasing  intensity.  During  this 
time  no  inspiratory  effort  is  made  and  as  the  result  of  the  expulsion  of 
the  air  from  the  lungs  there  are  signs  of  defective  aeration  of  the  blood. 
The  face  becomes  swollen  and  congested  or  it  may  be  deeply  cyanotic; 
the  veins  are  prominent  and  the  eyes  may  protrude  and  are  injected  and 
water}-.     The   symptoms   and   signs   are   those   of   asphyxiation.     The 

1  Jour.  Med.  Res.,  November,  1912. 


DISEASES    OF   THE   BRONCHI  269 

attack  terminates  with  a  long,  convulsive  inspiration  or  whoop;  occasion- 
ally the  fit  ends  with  sneezing.  The  seizure  lasts  from  a  few  seconds  to 
a  few  minutes. and  is  apt  to  be  more  frequent  at  night  than  during  the 
day.  Crying,  emotion  of  any  kind  or  the  inhalation  of  dust  often  pre- 
cipitates an  attack.  With  the  entrance  of  air  into  the  lungs  the  color  is 
restored  and  the  child  breathes  normally.  Vomiting  very  commonly 
follows  the  paroxysm  and  this  may  recur  so  often  that  the  child  becomes 
emaciated  from  lack  of  food.  Relaxation  of  the  vesical  and  rectal 
sphincters  may  occur  in  a  severe  paroxysm.  Occasionally  an  ulcer  is 
formed  on  the  under  surface  of  the  tongue  from  rubbing  on  the  teeth. 

Owing  to  the  intense  distress  the  child  learns  to  dread  succeeding 
attacks.  "At  first  he  tries  to  avert  the  paroxysm.  Instead  of  breathing 
naturally  and  expanding  his  lungs  to  the  full,  as  he  was  doing  just  before, 
he  holds  his  breath,  for  it  seems  to  him  that  the  full  current  of  air,  by 
entering  his  larynx,  will  produce  the  exhausting  cough  of  which  he  has 
had  a  sad  experience  ....  The  fit  takes  place.  You  at  once  see 
the  patient  look  around  for  a  support  to  which  he  may  cling.  If  he  is  a 
child  at  the  breast,  he  throws  himself  into  the  arms  of  his  mother  or 
nurse.  If  he  is  older  and  standing  up,  you  notice  him  stamping  in  a 
state  of  complete  distress.  If  he  is  lying  down,  he  sits  up  quickly  and 
clutches  hold  of  the  bed  curtains  or  of  the  rails"  (Trousseau1).  In  a  case 
of  ordinary  severity  there  are  usually  a  half  a  dozen  paroxysms  a  day. 
At  times  several  paroxysms  succeed  each  other  rapidly  until  some  tena- 
cious sputum  is  expelled.  Usually  this  consists  of  a  small  mass  or  shreds 
of  glairy  mucus.  In  very  severe  cases  there  may  be  a  paroxysm  every 
half  hour  and  death  may  result  from  exhaustion. 

In  unusually  severe  cases  rupture  of  the  capillaries  or  even  of  large 
blood-vessels  may  occur.  Epistaxis,  subconjunctival  bleeding,  hemop- 
tysis, convulsions  due  to  capillary  hemorrhages,  and  hemiplegia  have 
been  noted.  Rarely  death  takes  place  as  the  result  of  a  subdural  hemor- 
rhage. The  spasmodic  stage  may  terminate  within  three  weeks;  more 
often  it  lasts  for  four  or  five  weeks.  Occasionally  the  disease  seems  to 
become  more  or  less  chronic,  as  the  paroxysmal  stage  may  last  two  or 
more  months. 

The  third  stage  is  only  imperfectly  defined.  The  paroxysms  gradually 
decrease  in  number  and  severity,  especially  at  night.  The  cough  be- 
comes looser  and  the  sputum  becomes  mucopurulent  in  character.  In 
children  the  cough  may  persist  for  some  time  as  a  result  of  irritability 
of  the  larynx.  The  duration  of  the  disease  is  rarely  under  six  weeks. 
Occasionally  the  spasmodic  period  persists  for  two  months  or  more. 
The  complications  usually  manifest  themselves  during  the  stage  of 
decline. 

Complications  may  arise,  however,  during  the  paroxysmal  stage. 
Trousseau  expressed  the  opinion  that  when  it  is  noted  that  the  fits,  which 
have  been  numerous,  suddenly  cease,  an  inflammatory  complication  is 
to  be  suspected. 

Physical  Signs. — There  are  no  physical  signs  peculiar  to  whooping 
cough  other  than  the  change  in  the  character  of  respiration  during  the 
paroxysmal  stage.  In  the  catarrhal  stage  there  may  be  no  chest  signs 
whatever  or  there  may  be  rales  as  in  cases  of  simple  bronchitis.  During 
the  paroxysms  the  percussion  note  may  be  slightly  elevated  and  of  short 
1  "Clinical  Lectures,"  vol.  i,  New  Sydenham  Soc,  p.  664. 


270      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

duration  owing  to  the  diminished  air  content  of  the  lungs.  There  is  no 
inspiratory  sound  and  the  expiration  is  imperfectly  heard.  Following 
the  "whoop"  the  breath  sounds  are  distant  owing  to  the  gradual  ingress 
of  the  air.     A  few  rales  may  be  present. 

Diagnosis. — In  the  catarrhal  stage  the  diagnosis  is  not  possible 
although,  in  the  presence  of  an  epidemic  or  known  exposure,  the  possi- 
bility of  whooping  cough  should  suggest  itself.  Catarrhal  symptoms  also 
occur  as  prodromes  in  measles  and  as  these  two  infections  commonly 
precede  or  follow  each  other  both  should  be  kept  in  mind.  In  such 
cases  the  mouth  should  always  be  examined  for  Koplik's  spots. 

Once  the  " whoop"  has  appeared  the  diagnosis  is  easy.  In  doubtful 
cases,  especially  those  in  which  the  "whoop"  is  absent  or  not  character- 
istic, the  complement  fixation  test  may  aid  in  the  diagnosis. 

When  broncho-pneumonia  occurs  the  symptoms  and  physical  signs 
of  that  condition  dominate  the  picture.  A  very  serious  sequel  is  tubercu- 
losis. This  condition  is  to  be  suspected  in  children  who  are  delicate  and 
in  whom  fever  persists  and  emaciation  and  weakness  gradually  become 
more  and  more  marked.  In  these  cases  the  whooping  cough  serves  to 
arouse  into  activity  a  latent  tuberculous  process  already  present.  Many 
of  the  fatal  cases  of  broncho-pneumonia  following  pertussis  are  tubercu- 
lous in  character. 

BRONCHIAL  ASTHMA 

By  the  term  bronchial  asthma  is  meant  a  form  of  paroxysmal  dyspnea 
the  characteristic  feature  of  which  is  marked  diminution  or  arrest  of  the 
respiratory  movements  with  prolonged  expiration.  The  condition  is 
sometimes  referred  to  as  spasmodic  asthma.  Among  the  older  writers 
many  affections  characterized  by  paroxysmal  attacks  of  dyspnea  were 
referred  to  as  asthma,  often  having  the  prefix  cardiac,  renal,  etc.  The 
use  of  the  term  asthma  should  be  restricted  to  the  bronchial  type  of  the 
disorder. 

Etiology. — The  disease  may  manifest  itself  at  any  age,  but  shows  a 
decided  preponderance  in  favor  of  the  earlier  years  of  life.  The  follow- 
ing table  shows  the  age  distribution  in  225  cases  collected  by  Hvde 
Salter1: 

Cases  Per  cent. 

During  first  year 11  31.0 

From     1  to  10 60 

From  10  to  20 30  12.8 

From  20  to  30 39  17.0 

From  30  to  40 44  19.0 

From  40  to  50 24  9.0 

From  50  to  60 12  5.0 

From  60  to  70 4  1.7 

From  70  to  80 1  0.4 

In  regard  to  sex  males  are  more  subject  to  the  disease  than  females 
in  the  proportion  of  nearly  2  to  1. 

It  has  long  been  recognized  that  the  condition  is  often  hereditary. 
In  a  very  considerable  proportion  of  cases  there  is  a  direct  transmission  of 
the  predisposition  to  asthma  or  hay  fever,  the  latter  condition  being  closely 
allied  to  asthma  both  in  its  causation  and  in  its  clinical  manifestations. 

1  "Asthma,"  London,  1868. 


DISEASES    OF   THE  BRONCHI  271 

The  influence  of  climate  is  uncertain  although  in  most  instances  an 
asthmatic  is  less  subject  to  attacks  in  a  warm  equable  region  than  in 
one  which  is  cold  and  subject  to  marked  variations  in  the  temperature. 
In  regard  to  location  the  disease  often  manifests  the  most  curious  vagaries. 
I  once  knew  a  man  residing  in  a  city  not  far  removed  from  Philadelphia 
who  suffered  severely  from  asthma  and  who  became  free  from  his  attacks 
on  removing  to  the  latter  city.  In  such  cases  it  is  probable  that  some 
irritant,  to  which  the  individual  has  been  susceptible,  has  been  present 
in  one  place  and  not  in  the  other. 

In  certain  instances  the  asthmatic  attacks  seem  to  be  related  in 
some  way  to  the  presence  of  nasal  polypi,  nasal  spurs,  deviation  of  the 
nasal  septum  or  hypertrophy  of  the  turbinates.  Very  often  the  removal 
or  correction  of  these  defects  is  followed  by  a  disappearance  of  the 
asthmatic  attacks. 

It  is  a  matter  of  common  observation  that  asthmatics  rarely  develop 
tuberculosis  and  most  authorities  state  that  asthma  rarely  occurs  in 
tuberculous  individuals.  Occasionally,  however,  tuberculous  patients 
suffer  from  asthmatic  attacks  at  the  onset  of  or  during  the  course  of  their 
malady.     I  have  recently  seen  two  examples  of  this. 

Exciting  Causes. — In  practically  all  individuals  who  are  susceptible 
to  attacks  of  asthma  or  hay  fever  there  is  nearly  always  some  other 
factor  needed  to  precipitate  a  seizure.  The  immediate  causes  are  of  the 
most  diversified  nature.  Among  these  may  be  mentioned  chilling  of  the 
surface  of  the  body,  sudden  variations  of  the  weather  conditions,  over- 
eating, gastro-intestinal  disturbances,  uterine  disorders,  sudden  emotions 
such  as  anger  or  nervous  shock  and  lastly,  but  probably  of  more  im- 
portance than  all  the  others,  the  inhalation  of  various  kinds  of  dust  or 
odors. 

The  effect  of  the  inhalation  of  various  dusts  or  odors,  particularly 
the  odors  emanating  from  animals,  is  one  of  the  most  remarkable  features 
of  asthma.  In  one  individual  the  emanations  from  the  horse  provoke 
a  seizure ;  in  another  the  presence  of  a  cat  will  give  rise  to  an  attack ;  while 
in  still  others  rabbits  or  guinea-pigs  are  the  offending  animals.  A  medical 
friend  previously  free  from  the  disease,  always  developed  asthmatic 
attacks  after  a  visit  to  the  animal  room  of  the  laboratory  in  which  he 
worked.  Exposure  to  the  emanations  of  the  animals  even  for  a  few 
minutes,  would  lead  to  some  difficulty  in  breathing.  Not  knowing  which 
animal  was  the  cause  of  his  trouble  he  made  cutaneous  tests  with  the 
serum  of  the  different  animals.  The  serum  from  the  rabbit  gave  a  slight 
reaction,  while  that  from  the  guinea-pig  in  the  course  of  a  few  minutes, 
produced  at  the  site  of  the  inoculation,  a  marked  urticarial  swelling.  The 
skin  test  is  also  employed  in  the  case  of  hay  fever  patients  to  determine 
which  particular  pollen  is  the  offender. 

The  sensitiveness  of  many  individuals  to  the  pollen  of  various  weeds 
and  flowers  has  long  been  recognized  and  in  the  case  of  a  susceptible 
individual  the  inhalation  of  pollen  may  give  rise  to  an  attack  of  hay  fever 
or  asthma  or  both.  In  other  instances  the  inhalation  of  pungent  odors, 
such  as  that  given  off  by  mustard,  will  lead  to  an  attack.  Finally,  expo- 
sure to  an  excessive  amount  of  dust,  of  whatever  nature,  will  often  produce 
a  seizure. 

Hypotheses  as  to  the  Cause  of  Asthma. — Of  the  many  hypotheses  which 
have  been  advanced  to  explain  the  cause  of  an  asthmatic  attack  but  two 


272      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

are  worthy  of  serious  consideration,  namely:  (1)  spasm  of  the  circular 
fibers  of  the  bronchial  wall;  and  (2)  a  rapid  swelling  of  the  mucous  mem- 
brane of  the  bronchi.  While  the  first  hypothesis  is  the  one  most  gener- 
ally accepted  as  the  immediate  cause  of  the  attack  it  is  probable  that  the 
second  factor  also  plays  a  part  and  that  both,  rather  than. either  one 
alone,  are  concerned  in  producing  the  phenomena  of  an  asthmatic  seiz- 
ure. Asthma  is  caused  by  a  disturbance  of  function,  the  immediate 
manifestation  of  which  is  a  characteristic  form  of  paroxysmal  dyspnea. 
There  is  no  disease  of  the  bronchi  or  pulmonary  tissue,  although  repeated 
attacks  over  a  long  period  of  years  usually  lead  to  secondary  changes. 

The  most  rational  explanation  of  the  asthmatic  seizure  is  to  be  found 
in  the  phenomenon  of  anaphylaxis  which  may  be  produced  experimentally 
in  animals  by  the  injection  of  an  alien  proteid.  If,  for  instance,  a  guinea- 
pig  be  given  a  subcutaneous,  intraperitoneal  or  intravenous  injection  of 
normal  horse  serum,  and  then,  after  an  interval  of  ten  days  or  more  this 
injection  be  repeated,  it  is  found  that  in  the  elapsed  time  the  animal  has 
become  sensitized,  and  that  while  the  first  injection  has  been  without 
noticeable  harmful  effect,  the  second  injection  causes  a  very  violent 
poisoning.  Both  the  symptoms  and  the  anatomical  changes  resulting 
from  this  poisoning  are  predominantly  respiratory  in  nature.  An  ani- 
mal so  poisoned  will  within  a  minute  or  so  after  the  second  injection, 
vigorously  rub  its  nose,  frequently  give  a  spasmodic  sneeze  and  then 
begin  to  breathe  rapidly.  Quickly  following  this  it  is  noted  that  the 
sides  of  the  chest  sink  in  with  each  inspiration  and  finally  the  respira- 
tions become  very  slow  and  labored.  The  animal  shortly  shows  tonic 
and  clonic  convulsions,  the  mucous  membranes  of  the  mouth  and  tongue 
become  bluish  and  often  a  spurt  of  urine  is  seen.  After  a  brief  interval 
in  which  respiration  ceases  entirely  the  breathing  is  resumed,  the  respira- 
tions being  slow  and  causing  but  little  movement  of  the  chest;  gradually 
the  respirations  become  weaker  and  weaker  and  finally  cease  entirely. 
Auer  and  Lewis  state  that  the  characteristic  feature  of  anaphylaxis,  as 
seen  in  the  guinea-pig,  is  extreme  distention  and  immobilization  of  the 
lungs.     Anatomically  the  following  condition  is  found: 

"The  diaphragm  is  much  less  arched  than  in  normal  animals  after 
death.  On  opening  the  chest  the  lungs  present  a  striking  sight;  the 
lungs  do  not  collapse,  as  normal  lungs  do  when  the  thoracic  cavity  is 
opened,  but  remain  almost  fully  distended.  They  look  pale  bluish  pink, 
and  apparently  form  a  cast  of  the  thoracic  cavity.  Even  when  excised 
in  toto  there  is  practically  no  collapse  and  the  posterior  surfaces  often 
clearly  show  the  markings  of  the  ribs.  The  lungs  are  light,  soft  and 
spongy  and  float  on  water  like  a  cork.  On  cutting  away  pieces  of  lung 
tissue  these  pieces  do  not  collapse,  but  remain  distended;  the  cut  surface 
is  usually  dry  and  on  pressure  a  good  amount  of  air  may  be  expressed. 
Occasionally  this  pressure  reveals  some  small  foci  of  white  foam,  as  if 
there  were  beginning  pulmonary  edema;  occasionally  small  hemorrhages 
were  seen  on  the  surface  of  the  lungs.  The  trachea  and  bronchi  usually 
were  dry,  but  showed  often  a  marked  congestion  of  the  mucosa." 

The  explanation  of  this  extreme  inflation  of  the  lungs  in  association 
with  the  difficulty  in  breathing  is  to  be  ascribed  to  a  tetanic  contraction 
of  the  muscles  of  the  finer  bronchioles  so  that  the  air  is  imprisoned  in  the 
alveolar  sacs.  Auer  and  Lewis  state  that  the  anatomical  basis  for  this 
is  clear  and  that  the  condition  can  be  easily  recognized.     The  finer 


DISEASES    OF   THE   BRONCHI  273 

bronchioles  are  practically  nothing  but  muscular  tubes  and  muscle  fibers 
are  also  present  in  the  alveolar  ducts.  The  contraction  of  their  struc- 
ture, therefore,  must  have  a  profound  effect  upon  the  volume  of  air  pass- 
ing to  and  from  the  alveoli  and  the  condition  may  be  still  farther  aggra- 
vated by  submucous  edema  of  the  bronchi.  The  opportunity  to  examine 
the  lungs  of  an  individual  who  has  died  during  an  asthmatic  attack 
rarely  occurs  so  that  it  is  not  possible  to  compare  the  conditions  found  in 
man  and  experimental  animals  from  the  anatomical  standpoint.  We  do 
know,  however,  that  in  man  both  the  symptoms  and  physical  signs  point 
strongly  to  marked  over-distention  of  the  lungs;  that  the  air  is  taken  in 
with  difficulty  and  expelled  with  even  greater  difficulty;  and  that  the 
condition  abruptly  ceases  either  spontaneously  or  often  as  the  result  of 
an  injection  of  atropine.  Everything  points,  therefore,  to  spasm  of  the 
bronchioles  as  being  the  immediate  cause  of  the  phenomenon. 

Taking  up  next  the  exciting  cause  of  the  attack  it  will  be  recalled 
that  in  considering  the  etiology  we  pointed  out  that  an  asthmatic  seizure 
or  an  attack  of  hay  fever  was  often  precipitated  by  the  inhalation  of 
some  form  of  dust  or  animal  odor.  In  the  anaphylactic  phenomenon  as 
seen  in  animals,  "The  reaction  of  intoxication  would  seem  to  be  a  cellular 
one,  dependent  upon  a  heightened  power  of  assimilation  on  the  part  of 
cells  which  have  been  subjected  to  the  anaphylactic  substance  over  a 
definite  period  of  incubation"  (Gay  and  Southard).  As  a  general  rule 
we  have  no  knowledge  of  how  man  has  become  sensitized  to  various 
substances,  exposure  to  which  induces  an  attack.  That  sensitization 
has  taken  place,  however,  there  can  be  no  doubt  as  contact  with  certain 
animals,  the  inhalation  of  certain  pollens,  etc.,  promptly  induces  in  some 
individuals,  an  attack  of  asthma  or  hay  fever  or  both.  Attacks  which 
are  induced  by  overeating  or  constipation  may  also  be  explained  on  the 
ground  of  proteid  intoxication.  In  those  instances  in  which  attacks 
occur  in  one  locality  and  not  in  another  it  is  probable  that  the  particular 
substance  to  which  the  individual  is  sensitive  is  present  in  one  place  and 
not  in  another.  This  assumption  is  amply  borne  out  by  the  fact  that 
hay  fever  patients  either  escape  an  attack  entirely  or  have  their  symp- 
toms greatly  modified  by  residence  in  a  locality  which  is  free  from  the 
pollen  to  which  they  are  especially  susceptible. 

Finally,  we  have  to  consider  the  question  of  heredity  upon  which 
much  stress  has  been  laid.  If  we  accept  the  theory  that  the  primary 
cause  of  asthma  or  hay  fever  be  a  cellular  hypersensitiveness  to  certain 
substances,  it  can  easily  be  seen  that  this  sensitiveness  may  very  readily 
be  transmitted  from  parent  to  child.  And  here  again  the  experimental 
data  may  be  applied  to  the  disease  as  seen  in  man.  Thus  it  has  been 
shown  in  animals  that  if  the  female  be  sensitized  to  an  alien  proteid,  such 
as  normal  horse  serum,  susceptibility  to  this  proteid  is  transmitted  to 
her  offspring. 

Admitting  that  there  are  instances  in  which  it  is  not  possible  to  deter- 
mine the  exciting  cause  and  admitting  also  that  an  asthmatic  attack 
rarely  if  ever  ends  fatally  it  must  be  conceded  that  the  fulminant  type 
of  respiratory  distress  which  may  be  produced  experimentally  in  animals 
bears  a  close  analogy  to  the  asthmatic  seizures  which  occur  in  man. 

The  so-called  anaphylactic  reactions  of  asthma,  etc.,  are  commonly 
regarded  as  exceptional  and  pathological  events,  but  we  must  suspect 
a   qualitatively   similar,  if   quantitatively  different,  biological  response 

18 


274      DISEASES   OP  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

whenever  the  sensitized  being  breathes  air  containing  the  appropriate 
excitant   (Sewall). 

It  has  become  traditional  to  ascribe  to  the  majority  of  individuals  who 
suffer  from  asthma  or  hay  fever,  a  neurotic  tendency.  This  hypothesis 
it  seems  to  me  has  no  real  basis  in  fact  and  to  perpetuate  it  is  a  mistake. 

Symptoms. — The  essential  feature  of  asthma  is  a  paroxysmal  attack 
of  dyspnea.  The  attack  may  occur  with  explosive  suddenness  or  it  may 
be  preceded  by  premonitory  symptoms.  The  latter  are  varied  in  charac- 
ter and  occur  in  about  one-half  of  the  cases.  An  individual  subject  to 
the  disease  can  often  predict  an  attack  because  of  drowsiness,  neuralgia, 
itching,  irritability  or  sneezing.  In  other  instances  the  attack  is  pre- 
ceded by  flatulency  or  marked  diuresis.  I  have  already  referred  to  the 
role  played  by  odors,  exposure  to  which  will  bring  on  a  seizure  within  a 
a  few  minutes. 

The  first  evidence  of  the  attack  itself  is  a  feeling  of  tightness  or 
oppression  in  the  chest.  This  may  be  present  for  a  day  or  so  or  it  may 
manifest  itself  suddenly.  The  attack  may  occur  at  any  time  but  it  has 
long  been  noted  that  it  is  apt  to  manifest  itself  in  the  night.  The  patient 
goes  to  bed  feeling  perfectly  well,  when  he  is  suddenly  awakened  by  a 
feeling  of  suffocation  or  constriction  about  the  chest.  The  difficulty  in 
breathing  rapidly  increases  and  often  reaches  an  extreme  degree.  The 
face  is  pale  and  anxious  and  may  be  covered  with  a  cold  perspiration. 
Owing  to  the  deficient  oxygenation  of  the  blood  the  lips  are  usually  of 
a  dusky  hue  and  in  a  severe  attack  the  face  may  also  be  of  a  leaden  or 
dusky  color.  The  eyes  may  protrude  and  the  nostrils  may  be  dilated. 
In  the  effort  to  obtain  more  air  the  patient  may  rush  to  an  open  window. 
More  often,  however,  he  assumes  a  fixed  position.  This  may  be  standing 
up  with  the  hands  grasping  some  support  or  sitting  up  in  bed  with  the 
hands  pressed  upon  the  bed.  In  either  case  the  object  is  to  give  an  addi- 
tional purchase  to  the  accessory  muscles  of  respiration.  The  head  may 
be  thrown  back  or  it  may  be  thrust  forward  and  sunk  between  the 
shoulders,  "turtle-like." 

The  mechanical  difficulty  in  asthma  is  in  expelling  the  air  from  the 
lungs.  The  lungs  are  greatly  distended  and  owing  to  the  spasm  of  the 
finer  bronchi  the  air  vesicles  are  incapable  of  emptying  themselves. 
The  inspirations  are  reduced  in  frequency,  sometimes  to  one-half  the 
normal.  They  are  jerky  in  character  and  much  shortened  in  duration, 
the  normal  ratio  between  inspiration  and  expiration  being  in  extreme 
cases,  reversed.  In  spite  of  the  desperate  efforts  on  the  part  of  the  patient 
the  chest  scarcely  moves  because  the  lungs  are  already  fully  distended. 
The  supraclavicular  and  suprasternal  depressions  are  more  pronounced 
and  the  intercostal  spaces  are  sunken. 

During  the  attack  the  pulse  may  be  small  but  usually  it  is  but  little 
affected  and  the  temperature  is  normal. 

The  duration  of  an  attack  may  be  from  10  or  15  minutes  to  several 
days,  but  when  prolonged  beyond  several  hours  the  severity  of  the 
symptoms  is  usually  diminished. 

There  is  no  disease  in  which  during  the  height  of  an  attack,  the 
symptoms  are  so  distressing  and  alarming  and  yet  at  the  same  time  are 
so  free  from  danger.  Death  rarely,  if  ever,  occurs  as  the  result  of  an 
attack  of  spasmodic  asthma. 

There  may  be  a  short  dry  cough  at  the  onset  but  during  the  height 


DISEASES    OF  THE   BRONCHI  275 

of  the  attack,  cough  is  inconspicuous.  As  the  paroxysm  subsides  expec- 
toration usually  begins  and  this  is  attended  with  a  cough.  The  sputum 
at  first  occurs  in  the  form  of  small  grayish  pellets.  Later  it  gradually 
becomes  more  and  more  copious  and  also  changes  from  the  tenacious 
mucous  to  a  thin  frothy  material.  In  very  violent  attacks  the  sputum 
may  be  blood-streaked.  Any  considerable  amount  of  blood,  however, 
is  probably  an  indication  of  some  associated  pulmonary  lesion.  Micro- 
scopically the  sputum  is  seen  to  contain  many  eosinophiles,  Charcot- 
Leyden  crystals  and  Curschmann's  spirals. 

I  have  already  referred  to  the  close  relationship  which  exists  between 
bronchial  asthma  and  hay  fever.  Individuals  who  are  subject  to  hay 
fever  as  a  rule  suffer  no  inconvenience  except  during  the  fall  of  the  year 
when  exposure  to  various  pollens  is  common.  In  the  majority  of  hay 
fever  patients  the  symptoms  are  those  of  an  aggravated  attack  of  coryza. 
'In  addition  they  are  apt  to  be  subject  to  sneezing,  a  paroxysmal  cough 
and  considerable  depression.  Disturbance  of  the  respiratory  function 
varies  greatly.  It  may  consist  of  nothing  more  than  a  slight  feeling  of 
constriction  or  it  may  be  indistinguishable  from  true  asthma.'  Again, 
in  the  same  individual  the  coryza  symptoms  may  predominate  one  year 
while  at  another  time  the  asthmatic  symptoms  are  the  most  severe. 

Paroxysmal  attacks  of  sneezing  are  also  to  be  looked  upon  as  a  minor 
manifestation  of  irritation  of  the  finer  bronchi.  Finally,  there  is  to  be 
considered  urticaria  which  usually  occurs  alone  but  may  be  associated 
with  asthma.  It  will  be  recalled  that  urticaria  is  a  well-recognized 
anaphylactic  phenomenon  and  frequently  is  seen  after  the  injection  of  a 
foreign  proteid. 

Attacks  of  bronchial  asthma  may  occur  at  intervals  for  years  without 
producing  changes  in  the  bronchi  or  pulmonary  tissue.  Cases  of  this 
type  are,  as  a  rule,  those  which  arise  as  the  result  of  exposure  to  some 
irritant  such  as  the  pollen  of  flowers  or  weeds  or  animal  odors.  In  many 
instances,  however,  the  attacks  occur  early  in  life  and  tend  to  increase 
in  severity.  Under  these  circumstances  the  individual  becomes  definitely 
"asthmatic."  Both  the  severity  and  the  duration  of  the  seizures  gradu- 
ally bring  about  permanent  over-distention  of  the  lungs  so  that  in  addi- 
tion to  being  subject  to  attacks  of  spasmodic  dyspnea  the  individual 
becomes  emphysematous. 

Physical  Signs. — Inspection.- — The  general  features  of  an  attack  of 
asthma  have  been  dealt  with  in  describing  the  symptoms.  The  physical 
appearance  of  the  patient  will  depend  largely  on  the  duration  of  the 
disease.  If  chronic  and  of  long  standing  the  chest,  as  a  result  of  the 
associated  emphysema,  will  present  the  characteristic  barrel  shape  of 
the  latter  disease.  On  the  other  hand,  those  who  suffer  from  asthmatic 
attacks  only  occasionally,  or  who  have  but  recently  developed  the  disease, 
will  show  no  change  in  the  contour  of  the  chest. 

During  an  attack  there  are  two  striking  features  to  be  noted  by 
inspection:  (1)  The  over-distention  of  the  chest,  and  (2)  the  very 
slight  expansile  movement  of  the  thorax.  This  is  in  striking  contrast  to 
the  forcible  action  of  the  accessory  muscles  of  respiration.  The  dia- 
phragm is  depressed  and  the  abdominal  muscles  rigid.  During  inspira- 
tion, which  is  short  and  quick,  the  intercostal  spaces  are  drawn  in.  In 
most  cases  the  prolongation  of  expiration  is  apparent  on  inspection. 

Palpation. — This  confirms  the  deficiency  of  the  expansible  movement 


276      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

of  the  chest  noted  on  inspection.  Vocal  resonance  may  be  normal  but 
if  the  attack  is  a  severe  one  it  may  be  greatly  diminished  partly  because 
of  the  over-distended  lung  and  partly  because  of  the  inability  of  the 
patient  to  speak  loudly. 

Percussion.- — On  percussion  the  note  will  vary  from  that  which  is 
normal  to  one  which  is  markedly  hyperresonant.  The  degree  of  exaggera- 
tion of  the  resonant  quality  of  the  percussion  note  depends  on  the  amount 
of  associated  emphysema.  If  the  latter  condition  is  a  prominent  feature 
the  percussion  note  will  be  hyperresonant  all  over  the  chest  and  the 
area  of  cardiac  dulness  absent. 

Auscultation. — During  the  height  of  the  attack  the  vesicular  murmur 
is  usually  inaudible  and  instead  a  to-and-fro  wheezing  sound  is  heard. 
As  the  attack  begins  to  subside  innumerable  rales  are  heard  throughout 
the  chest.  At  first  the  rales  are  sibilant  and  sonorous  in  character  and 
may  be  both  low-  and  high-pitched.  Later  fine  moist  crepitant  and 
subcrepitant  rales  are  heard,  especially  over  the  lower  portions  of  the 
lungs.  The  short,  jerky  character  of  the  inspiratory  effort  and  the  pro- 
longation of  the  expiratory  act  are  plainly  evident  on  auscultation.  The 
vocal  fremitus  may  be  normal  or  exaggerated,  but  as  a  rule  the  distress 
of  the  patient  is  such  that  the  use  of  the  voice  is  not  attempted. 

Diagnosis. — The  term  asthma  should  be  restricted  to  that  form  of 
spasmodic  dyspnea  in  which  the  chief  feature  is  the  difficulty  in  emptying 
the  lungs,  that  is.  it  is  an  expiratory  form  of  dyspnea.  In  all  other  forms 
of  dyspnea  the  principal  difficulty  is  in  getting  air  into  the  lungs.  In 
those  instances  in  which  there  is  an  obstruction  in  the  upper  respiratory 
tract  there  may  be  trouble  both  in  inspiration  and  expiration.  Obstruc- 
tion most  commonly  occurs  in  the  larynx  or  trachea  and  may  be  brought 
about  by  edema  of  the  larynx,  diphtheria,  inflammatory  swelling  of  the 
larynx  due  to  some  irritant  or  the  obstruction  may  result  from  pressure 
without  as  by  tumors,  enlarged  lymph  nodes  or  a  thoracic  aneurism. 
In  such  cases  the  dyspnea  is  usually  quite  plainly  inspiratory  in  character 
and  is  also  apt  to  be  accompanied  by  a  stridor.  Aphonia  due  to  paralysis 
of  the  vocal  cords  may  occur  also.  These  cases,  as  a  rule,  offer  no  diffi- 
culty, but  in  an  individual  suffering  from  the  first  asthmatic  attack,  the 
various  causes  of  dyspnea  should  be  borne  in  mind. 

Cases  of  chronic  heart  disease  frequently  suffer  from  dyspnea.  In 
some  instances  the  dyspnea  may  appear  suddenly  and  in  a  paroxysmal 
form.  The  inspiration  is  free,  and  the  expiration  is  not  prolonged. 
Examination  of  the  heart  will  give  the  correct  clue  to  the  origin  of  the 
trouble.  Attacks  of  paroxysmal  difficulty  in  breathing  which  appear 
first  after  middle  life  are  quite  commonly  cardiac  in  origin.  In  some  of 
these  cases  the  dyspnea  is  enhanced  by  the  coincident  presence  of 
acidosis. 

Attacks  of  dyspnea,  sometimes  characterized  by  a  sudden  onset  are 
not  infrequent  in  cases  of  nephritis.  The  presence  of  edema,  a  high 
blood-pressure,  a  ringing  second  aortic  sound  and  the  urinary  findings 
serve  to  establish  the  true  nature  of  the  dyspnea. 

BRONCHIECTASIS 

In  individuals  who  have  suffered  from  one  of  the  various  inflam- 
matory affections  of  the  lungs  or  bronchi  some  degree  of  bronchial  dila- 
tation is  not  an  infrequent  finding  in  the  autopsy  room.     The  usual 


DISEASES    OF   THE   BRONCHI  277 

teaching  is  that  clinically  bronchiectasis  is  relatively  uncommon.  This, 
I  believe,  to  be  a  mistake.  The  currently  accepted  view  that  bronchiec- 
tasis is  always  characterized  by  large  quantities  of  very  foul  smelling 
sputum  and  that  it  is  almost  invariably  an  affection  of  the  lower  lobes, 
must  be  revised.  As  a  rule,  only  those  cases  are  recognized,  in  which 
the  condition  has  become  distinctly  apparent  and  in  which  the  symptoms 
are  typical;  and  even  in  these  cases  the  true  nature  of  the  trouble  is 
often  overlooked  in  the  belief  that  tuberculosis  is  present. 

Etiology. — Dilatation  of  the  bronchi  is  practically  always  a  secondary 
affection  and  may  be  traced  to  some  preceding  disease  of  the  bronchi, 
lungs  or  pleurae.  In  the  great  majority  of  cases  of  bronchiectasis  the 
condition  is  chronic  and  its  evolution  gradual.  Occasionally  it  is  met 
with  in  an  acute  form. 

In  considering  the  exciting  factors  the  classification  suggested  by 
Fowler1  is  the  most  satisfactory. 

A.  Intrinsic,  or  conditions  acting  directly  through  the  bronchi. 

1.  Bronchitis,  acute  or  chronic.  The  chronic  form  of  bronchitis  is 
most  likely  to  lead  to  bronchiectasis  as  the  long-standing  inflammatory 
process  tends  to  weaken  the  bronchial  wall.  As  the  result  of  severe 
attacks  of  coughing  the  weakened  wall  is  unable  to  resist  the  pressure  of 
air  and  hence  the  bronchi  dilate.  Another  factor  is  the  mechanical 
plugging  of  the  bronchioles  by  the  catarrhal  secretions.  A  slight  degree 
of  dilatation  of  the  bronchi  is  not  infrequently  met  with  in  cases  of  emphy- 
sema and  asthma  owing  to  the  fact  that  those  two  pulmonary  affections 
are  almost  constantly  associated  with  a  chronic  bronchitis. 

In  my  experience  one  of  the  most  frequent  causes  of  bronchiectasis 
is  the  prolonged  exposure  to  inorganic  dust.  At  first  the  dust  produces  an 
irritation  of  the  mucous  membrane  of  the  upper  respiratory  tract.  Later 
it  induces  a  subacute  inflammation  of  the  bronchial  mucous  membrane 
and  in  addition  leads  to  connective  tissue  proliferation  in  the  interlobular 
septa.  Of  21  potters  whom  I  have  had  under  observation  the  evidences 
of  dilatation  of  the  bronchi  were  present  in  10.  Dilatation  of  the 
bronchi  has  also  been  noted  very  frequently  in  cases  of  anthracosis. 

Of  the  microorganisms,  the  influenza  bacillus  seems  to  be  the  most 
important  as  a  causative  agent. 

2.  Narrowing  of  the  lumen  of  the  bronchus.  This  may  be  caused 
by  a  gumma,  a  foreign  body,  or  by  pressure  from  without  as  in  the  case 
of  an  aneurism  or  a  tumor.  As  the  result  of  the  stricture  the  bronchial 
secretions  accumulate,  changes  in  the  bronchi  and  peribronchial  tissues 
take  place  and  the  surrounding  pulmonary  tissue  becomes  indurated. 
These  conditions  tend  to  weaken  the  bronchial  wall  and  if  there  be  added 
violent  expiratory  efforts  dilatation  ensues. 

Chevalier  Jackson'2  has  emphasized  the  importance  of  bearing  in  mind 
that  a  foreign  body  is  often  the  cause  of  bronchiectasis.  For  this  reason, 
all  cases  of  bronchiectasis  of  the  lower  lobes  should  have  an  X-ray 
examination  made. 

B.  Extrinsic,  or  causes  external  to  the  bronchus. — While  dilatation  can 
occur  as  the  result  of  changes  in  the  bronchus  alone  the  condition  is 
more  apt  to  develop  if  there  are,  in  addition,  associated  changes  in  the 
pulmonary  tissues. 

1  Fowler  and  Godlee  :  "  Diseases  of  the  Lungs,"  1898. 

2  Penna.  Med.  Jour.,  August,  1916. 


278      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

(a)  Tuberculosis. — In  a  very  considerable  number  of  cases  of  chronic 
ulcerative  tuberculosis  some  dilatation  of  the  bronchi  is  encountered, 
although  this  is  usually  not  recognized  clinically.  The  more  chronic 
the  tuberculosis  and  the  greater  the  amount  of  fibrous,  tissue  present, 
the  more  certain  is  there  to  be  some  evidence  of  bronchiectasis.  In 
197  consecutive  cases  autopsied  at  the  Phipps  Institute  the  bronchi  were 
noted  as  being  dilated  in  the  upper  lobes  in  20  instances;  in  the  middle 
lobe  of  the  right  lung  9  times  and  in  the  lower  lobes  9  times.  In  6 
additional  cases  the  dilatation  was  sufficiently  marked  to  constitute  a  true 
bronchiectasis;  of  this  number  4  occurred  in  the  lower  lobes. 

(b)  Syphilis  may  cause  dilatation  of  the  bronchi  in  one  of  two  ways: 
(1)  In  the  form  of  a  gumma  obstructing  the  lumen  of  the  bronchus.  This 
has  been  considered  among  the  intrinsic  causes.  (2)  The  occurrence  of 
pulmonary  fibrosis  as  the  result  of  syphilis.  L.  A.  Conner1  in  a  study 
of  syphilitic  stenosis  of  the  trachea  and  bronchi  found  that  bronchiectasis 
did  not  occur  in  more  than  20  per  cent,  of  the  cases.  Just  as  in  tubercu- 
losis and  other  chronic  pulmonary  affections  he  considered  that  "much 
more  potent  factors  are  the  changes  occurring  in  the  bronchial  wall  and 
in  the  adjacent  lung  tissue,  by  which  the  muscular  and  elastic  tissue  of 
the  bronchi,  upon  which  their  strength  and  resilience  depend,  is  replaced 
by  inflammatory  tissue." 

(c)  Compression  of  the  Lung. — The  most  frequent  cause  of  compres- 
sion of  the  lung  is  a  pleural  effusion,  either  serous  or  purulent  in  character. 
If  the  effusion  is  unrecognized  and  the  lung  remains  compressed  for  some 
time  a  proliferation  of  connective  tissue  takes  place  in  the  collapsed  lung 
and  the  bronchi  also  dilate.  It  is  probable  that  the  dilatation  occurs, 
more  as/the  result  of  the  distending  force  of  the  cough,  acting  on  bronchi 
deprived  of  their  normal  support,  rather  than  the  associated  fibroid 
changes  in  the  lung. 

(d)  Croupous  and  Broncho-pneumonia. — Although  delayed  resolution 
following  croupous  pneumonia  is  frequently  given  as  one  of  the  exciting 
causes  of  pulmonary  fibrosis  and  bronchiectasis,  there  is  some  question 
as  to  whether  sucha  thing  as  "delayed  resolution"  ever  occurs.  If  it 
does  it  is  extremely  rare.  In  the  vast  majority  of  instances  what  is 
taken  for  delayed  resolution  is  in  reality  an  effusion.  As  a  result  the 
lung  becomes  compressed  and  if  the  compression  is  exerted  sufficiently 
long,  pulmonary  fibrosis  and  dilatation  of  the  bronchi  ensue. 

Bronchial  dilatation,  in  some  instances,  apparently  originates  in  an 
attack  Of  broncho-pneumonia.  Under  these  circumstances  the  dilata- 
tion seems  to  arise  partly  as  the  result  of  the  associated  inflammatory 
condition  of  the  bronchi  and  adjacent  alveoli  and  partly  as  the  result 
of  collapse  of  air  vesicles  adjacent  to  the  pneumonic  process.  As  a  rule 
the  collapsed  vesicles  become  reexpanded  after  recovery  from  the  acute 
attack.  If,  however,  the  change  is  permanent  the  atelectatic  areas 
undergo  a  fibroid  change  and  the  smaller  bronchi  dilate. 

(e)  Fibrosis  of  the  Lung. — This  will  be  considered  in  detail  under 
another  heading.  It  may  be  stated  here,  however,  that  in  practically 
every  case  in  which  there  is  an  overgrowth  of  fibrous  tissue  in  the  lungs, 
there  is  also  dilatation  of  the  bronchi. 

(b)  Inflammation  of  the  Pleura. — Marked  thickening  of  the  pleura 
is  a  frequent  finding  in  cases  of  bronchiectasis.     Some  observers  hold  the 
1  Am.  Jour.  Med.  Sc,  1905,  vol.  cxxx. 


DISEASES    OF    THE   BRONCHI 


279 


view  that  a  chronic  adhesive  pleurisy  is  one  of  the  factors  capable  of 
bringing  about  dilatation  of  the  bronchi,  but  this  is  difficult  to  prove. 
Inasmuch  as  the  two  conditions  not  infrequently  occur  independently 
of  each  other,  it  is  quite  probable  that  when  they  are  associated  they 
have  nothing  in  common. 

A  consideration  of  the  above  etiological  factors  shows  that  while 
weakening  of  the  bronchial  wall  is  the  essential  feature  in  all  cases  that, 
as  a  rule,  one  or  more  additional  factors  are  at  work  in  any  given  case. 
Besides  disease  of  the  bronchial  walls,  therefore,  the  effect  of  increased 
intrapulmonary  pressure,  the  pressure  of  accumulated  secretions  within 
the  bronchi,  and  various  chronic  affections  involving  the  parenchyma  of 
the  lung,  are  also  to  be  taken  into  consideration. 


Fig.  221.- 


-Fibrosis  of  the  right  upper  lobe  with  dilatation  of  the  bronchi, 
would  give  the  signs  of  a  cavity. 


Such 


Morbid  Anatomy. — Although  at  the  autopsy  table  a  large  number 
of  the  tubes  are,  as  a  rule,  found  to  be  affected,  the  disease  in  the  early 
stage  is  much  more  limited.  The  successive  involvement  of  previously 
healthy  tubes  is  brought  about  by  the  inhalation  of  the  secretions,  inter- 
current attacks  of  bronchitis,  septic  broncho-pneumonia  and  frequent 
cough.  The  condition  may  be  limited  to  one  lung  or  both  may  be 
affected.     In  35  cases  seen  in  the  Brompton  Hospital,  Fowler  states  thaC 


280       DISEASES    OF   THE  BRONCHI,    LUNGS,    PLEURA,    AND   DIAPHRAGM 

in  23  cases  (or  65  per  cent.)  both  lungs  were  affected;  the  lesion  was 
limited  to  one  lobe  in  only  8.  In  52  autopsies  Lebert  found  that  the 
condition  was  limited  to  one  lung  in  52  per  cent,  and  that  in  48  per  cent, 
both  were  involved.  It  is  usually  believed  that  the  lower  lobes  are  most 
commonly  involved  and  that  localized  dilatation  of  the  bronchi  in  the 
apices  of  the  lungs  is  unusual.  Lebert,  however,  found  unilateral  upper 
lobe  involvement  in  11  per  cent,  of  his  cases.  In  chronic  non-tuberculous 
affections  bilateral  involvement  is  the  most  frequent  while  in  tuberculous 
cases  unilateral  and  apical  involvement  is  the  most  common.  Apical 
involvement  is  also  quite  common  in  cases  of  pneumoconiosis.     McCrae 


Fig.   222. — The  bronchiectatic  cavities  have  been  laid  open,  revealing  their  wide  extent 
and  intercommunication.      {Jefferson  Medical  College  Museum.) 

and  Funk1  have  reported  5  cases  of  apical  bronchiectasis,  4  of  which 
were  associated  with  tuberculosis  (see  Fig.  221). 

Two  main  varieties  of  bronchiectasis  are  recognized,  namely,  the 
cylindrical  and  the  globular  or  sacculated. 

In  the  cylindrical  form  the  dilatation  is  uniform,  the  smaller  bronchi 
retaining  the  size  of  the  larger  division  instead  of  diminishing  in  diameter. 
The  bronchi  tend  to  progressively  increase  in  size  toward  their  terminal 
extremities,  thus  giving  rise  to  an  appearance  resembling  that  of  the 
fingers  of  a  glove  (Wilson  Fox) .  This  type  of  the  disease  is  well  illustrated 
in  Fig.  222.  A  subvariety  of  the  cylindrical  form  is  the  fusiform  type,  in 
which  the  dilated  bronchi  taper  somewhat  toward  their  terminal  extremity. 

1  Jour.  Am.  Med.  Assoc,  Oct.  7,  1916. 


Fig.  223. — Cornification  of  the  lung  with  dilatation  of  the  bronchi  as  the  prominent 
feature.  This  lung  on  section  presented  the  appearance  of  a  series  of  coalesced  rings 
measuring  from  5  to  15  mm.  in  diameter.      (Case  No.  4702,  Phipps  Institute.) 


DISEASES    OF    THE    BRONCHI 


281 


The  sacculated  type  shows  the  most  extreme  degree  of  dilatation. 
In  this  form  the  tube  may  dilate  at  a  single  point,  forming  a  pseudo- 
cavity.  A  number  of  these  may  occur  in  one  tube,  the  caliber  of  the  inter- 
vening portions  remaining  approximately  normal.  The  sacculation 
may  involve  only  one  side  of  the  tube,  the  remainder  of  the  circumference 
retaining  its  normal  shape.  A  subvariety  of  the  sacculated  form  is 
that  in  which  the  affected  bronchus  presents  a  number  of  bead-like  dila- 
tations which  have  been  likened  to  a  rosary  (Fox). 


Fig.  224. — An  unusual  example  of  fibroid  phthisis  with  extensive  dilatation  of  the  bronchi. 

(Pennsylvania  Hospital.) 

The  cylindrical  type  of  dilatation  is  usually  found  in  the  larger  and 
medium-sized  tubes.  While  the  sacculated  type  may  occur  in  the 
larger  tubes,  it  is  most  commonly  encountered  in  the  terminal  bronchi. 
All  types  of  dilatation  may  be  seen  in  one  lung. 

The  largest  and  most  extensive  bronchiectases  are  encountered  in 
lungs  which  have  undergone  marked  fibroid  changes  (see  Figs.  223  and., 
224). 


282       DISEASES    OF   THE  BRONCHI,    LUNGS,    PLEURA,    AND   DIAPHRAGM 

Associated  Changes  in  the  Lungs. — The  pulmonary  changes  have 
been  very  tersely  expressed  by  Walshe  as  follows:  "The  surrounding 
tissue  is  either  slightly  condensed  by  pressure,  hardened  by  chronic 
pneumonia,  rarefied  by  emphysema  or  perfectly  natural."  A  septic 
broncho-pneumonia  due  to  inhalation  of  the  secretions  is  not  an  infre- 
quent terminal  event  and  occasionally  gangrene  of  the  lung  occurs  as 
the  result  of  perforation  of  the  bronchial  dilatation. 

Changes  in  Other  Organs. — Dilatation  of  the  right  heart  may  occur  as 
the  result  of  the  obstructed  circulation  in  the  lungs.  Owing  to  the  stag- 
nation of  septic  material  in  the  bronchial  tubes  the  absorption  of  toxins 
frequently  leads  to  amyloid  change  in  the  liver  and  kidneys.  Abscess 
of  the  brain  not  infrequently  has  its  origin  in  a  bronchiectasis. 

Changes  in  the  Extremities. — One  of  the  peculiar  features  of  the  disease 
is  the  remarkable  change  which  takes  place  in  the  extremities.  While 
clubbing  of  the  fingers  and  toes  occurs  in  other  conditions,  it  is  seen  in 
its  most  extreme  form  in  bronchiectasis.  And  the  same  is  true  of  hyper- 
trophic pulmonary  osteoarthropathy.  These  two  conditions,  which  are 
almost  exclusively  associated  with  diseases  of  the  lungs,  will  be  considered 
under  a  separate  heading. 

Symptoms. — It  can  be  readily  understood  that  the  symptoms  vary 
greatly  in  different  cases.  In  many  instances  the  symptoms  are  so 
slight  or  are  so  masked  by  associated  changes  in  the  bronchi  or  lungs 
that  the  presence  of  bronchiectasis  is  not  even  suspected.  Keeping  in 
mind  the  various  conditions  with  which  the  condition  is  commonly  asso- 
ciated will  often  lead  to  a  correct  diagnosis.  In  a  small  proportion  of 
cases  the  diagnosis  can  be  made  from  the  presence  of  two  symptoms, 
namely,  a  paroxysmal  cough  which  may  occur  but  two  or  three  times  a 
day  and  the  expectoration  of  large  quantities  of  purulent  sputum  which 
may,  in  some  cases,  be  horribly  fetid.  Coughing  paroxysms  are  most 
marked  in  the  morning  and  again  at  night  when  the  patient  lies  down. 
This  often  serves  to  empty  the  cavities  and  it  is  not  until  they  again  fill 
up  that  the  paroxysm  is  repeated.  The  sputum  may  be  raised  easily  or 
it  may  be  brought  up  only  after  a  severe  coughing  attack. 

The  sputum,  which  may  amount  to  20  ounces  or  more  in  24  hours,  is 
usually  yellowish  in  color  and  on  standing  separates  into  three  layers. 
The  lower  layer  is  opaque  and  grayish  in  color;  the  middle  consists  of  a 
thin,  turbid  fluid,  and  on  top  of  this  is  a  frothy,  brownish-colored  layer. 

In  cases  of  long  duration  the  sputum  often  has  a  horribly  fetid  odor. 
There  is  probably  no  disease  in  which  the  sufferer  becomes  such  an  ob- 
ject of  aversion  to  his  family  as  bronchiectasis.  I  recall  one  patient,  a 
lad  of  seventeen,  who  practically  became  an  outcast  because  of  his 
affliction.  In  this  case  the  whole  house  became  permeated  with  the 
gangrenous  odor  of  his  sputum  after  a  coughing  attack.  In  another  case 
in  which  the  bronchiectatic  cavities  were  emptied  during  the  adminis- 
tration of  an  anesthetic,  the  odor  was  so  nauseating  that  several  of  the 
onlookers  vomited  at  once. 

Sputum  of  the  type  described  is  not  by  any  means  the  rule,  however. 
Among  a  very  considerable  number  of  cases  of  bronchiectasis  I  have 
seen  there  were  but  four  or  five  in  which  the  sputum  was  fetid.  It  is 
rarely  so  if  the  bronchiectasis  is  confined  to  the  apices  as  the  drainage 
is  freer  and  the  secretions  do  not  stagnate  in  the  bronchi. 

Blood-streaked  sputum  and  even  small  hemoptyses  are  of  not  in- 


DISEASES    OF   THE   BRONCHI  283 

frequent  occurrence  and  occasionally  death  is  produced  by  a  large  pul- 
monary hemorrhage.  The  smaller  hemorrhages  are  due  to  ulceration 
of  the  bronchial  wall;  the  larger  ones  to  an  erosion  of  a  branch  of  the 
pulmonary  artery.  Dyspnea  is  usually  a  prominent  symptom  when  the 
disease  becomes  well  established.  It  may  be  due  to  a  variety  of  causes; 
dilatation  of  the  right  side  of  the  heart,  emphysema,  extensive  fibrosis 
of  the  lung,  fixation  of  the  diaphragm,  etc. 

Pain  may  occur  during  the  course  of  the  disease  from  extension  of 
the  pleural  inflammation. 

As  the  disease  progresses  circulatory  disturbances  are  apt  to  become 
more  and  more  marked  until  finally  all  the  evidences  of  failing  compen- 
sation develop. 

In  spite  of  the  large  amount  of  septic  material  which  is  more  or  less 
constantly  stagnating  in  the  bronchi,  constitutional  symptoms  are  not 
marked.  As  a  rule  cases  of  bronchiectasis  are  afebrile  although  they  are 
apt,  at  times,  to  have  periods  of  fever  due  to  intercurrent  attacks  of  bron- 
chitis or  broncho-pneumonia  as  the  result  of  the  invasion  of  a  new  area  of 
bronchial  or  pulmonary  tissue.  During  these  attacks  the  cough  is  more 
severe  and  night  sweats  commonly  occur. 

For  varying  periods  of  time  the  general  health  is  little  if  any  impaired 
but  as  time  goes  on  there  is  a  gradual  deterioration  in  strength  and 
nutrition  and  finally  death  ensues  as  the  result  of  cardiac  failure,  general 
cachexia,  or  some  terminal  infection. 

Physical  Signs. — Inspection. — Extreme  clubbing  of  the  fingers  is 
so  commonly  associated  with  dilatation  of  the  bronchi  as  to  be  of  decided 
value  in  diagnosis.  The  toes  may  be  clubbed  also  and  in  some  instances 
the  end  of  the  nose  becomes  bulbous  in  appearance. 

Owing  to  the  fact  that  dilatation  of  the  bronchi  is  secondary  to  such 
a  variety  of  diseases  and  the  changes  produced  by  these  diseases  are  so 
diverse  in  character,  the  physical  signs  vary  tremendously.  In  some 
instances  the  bronchiectasis  is  deep  seated  and  gives  rise  to  no  signs  what- 
soever. A  case  of  this  type  was  seen  recently  at  the  Phipps  Institute. 
The  patient  complained  of  cough  and  expectoration  but  the  examination 
of  the  chest  failed  to  reveal  any  abnormality.  Several  weeks  later  the 
patient  died  as  the  result  of  a  brain  abscess.  At  the  autopsy  deep-seated 
dilatation  of  the  bronchi  was  found  in  the  lower  lobe  of  the  right  lung. 

The  cases  which  most  frequently  escape  detection  are  those  in  which 
the  affection  is  bilateral  and  associated  with  chronic  bronchitis,  emphy- 
sema, or  diffuse  bilateral  fibrosis  of  the  lungs;  or  in  which  tuberculosis 
and  bronchiectasis  coexist.  In  these  cases  the  emphysema  or  tuber- 
culosis tends  to  mask  the  bronchial  affection.  The  condition  may  be 
suspected  if  marked  clubbing  of  the  fingers  is  present,  in  what  seems  to 
be  a  case  of  emphysema,  or  if  cavity  signs  are  more  marked  in  the  lower 
lobes. 

In  the  bilateral  cases,  the  chest  shows  no  discrepancy  between  the 
two  sides;  it  may  be  normal  in  appearance  or  of  the  emphysematous 
type. 

The  type  of  bronchiectasis  which  is  most  frequently  recognized  is  that 
which  involves  a  part  or  all  of  one  lung.  In -these  cases  there  is  marked 
retraction  of  the  affected  side  and  expansion  is  greatly  diminished  or 
entirely  absent.  The  heart  is  usually  displaced  towards  the  affected 
side. 


284       DISEASES   OF   THE  BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Palpation— If  emphysema  is  present  the  tactile  fremitus  is  reduced. 
In  unilateral  involvement  associated  with  pulmonary  fibrosis  the  fremitus 
is  increased. 

Percussion. — The  character  of  the  percussion  note  will  depend  almost 
entirely  on  the  nature  of  the  associated  pulmonary  changes  and  the 
location  of  the  dilatations.  In  deep-seated  bronchiectases  without  any 
change  in  the  parenchyma  of  the  lung,  the  note  is  normal ;  if  emphysema 
is  present,  it  is  hyperresonant,  and  if  consolidation  has  occurred  as  the 
result  of  a  chronic  interstitial  pneumonia,  the  note  will  be  dull. 

When  the  disease  is  confined  to  one  side  the  opposite  lung  is  usually 
hypertrophied  as  the  result  of  compensatory  emphysema.  This  is  in- 
dicated by  the  fact  that  the  pulmonary  resonance  extends  beyond  the 
middle  line  anteriorly;  in  addition  loud  puerile  breathing  will  be  heard 
on  this  side. 

Superficially  placed  dilatations  will  give  rise  to  a  high-pitched  tym- 
panitic note.  If  the  dilatations  are  numerous  a  distinct  tympanitic 
quality  may  be  lacking  but  will  influence  the  other  percussion  changes 
by  raising  the  pitch.  In  unilateral  cases  the  area  about  the  angle  of  the 
scapula  is  where  one  is  most  apt  to  elicit  a  tympanitic  note. 

Auscultation. — The  auscultatory  signs  present  the  greatest  variations. 
If  the  condition  is  bilateral  the  respiratory  sounds  may  be  identical  with 
those  heard  in  emphysema  or  they  may  be  slightly  suppressed  with  a 
bronchovesicular  quality,  especially  during  expiration.  In  the  unilateral 
cases  associated  with  fibrosis,  the  breath  sounds  are,  for  the  most  part, 
suppressed  but  in  certain  areas  are  definitely  cavernous.  The  latter 
type  of  breathing  is  very  frequently  heard  at  the  angle  of  the  scapula. 
Over  the  area  in  which  cavernous  breathing  is  heard  bronchophony  and 
whispering  pectoriloquy  may  be  marked.  Skoda's  veiled  puff  is  often 
referred  to.  This  sound  occurs  at  the  end  of  inspiration  and  sounds  as 
though  a  puff  of  air  were  entering  a  cavity  situated  just  beneath  the  ear. 
In  my  experience  this  sign  is  not  often  present. 

Rales  of  every  description  may  be  heard.  When  coarse  and  metallic 
in  quality  they  are  strongly  suggestive  of  cavity  formation  or  bronchial 
dilatation. 

A  systolic  murmur  at  the  base  of  the  heart  is  frequently  present.  In 
the  later  periods  of  the  disease  a  mitral  murmur  of  relative  insufficiency 
is  often  present  in  addition  to  other  evidences  of  failing  compensation. 

Diagnosis. — In  view  of  the  number  of  diseases  associated  with 
bronchiectasis  it  is  not  surprising  that  the  condition  is  so  frequently 
overlooked  clinically.     The  following  conditions  must  be  considered: 

Tuberculosis. — If  the  bronchiectasis  occurs  in  the  lower  lobes  there 
should  be  no  confusion  as  tuberculosis  almost  invariably  starts  at  the 
apex  and  extends  downward.  If  the  bronchi  of  the  upper  lobe  are 
dilated  it  is  not  possible  to  distinguish  the  two  conditions,  inasmuch  as 
a  tuberculous  excavation  and  the  dilated  bronchi  give  rise  to  the  same 
physical  signs.  Fig.  221  illustrates  very  clearly  how  a  mistake  might 
occur.  When  one  entire  lung  is  involved  or  both  lungs  are  implicated 
the  true  nature  of  the  trouble  cannot  be  determined  without  a  sputum 
examination;  and  in  any  case  this  always  should  be  done.  The  ma- 
jority of  mistakes  are  due  to  neglect  of  this  simple  procedure.  In 
examining  the  sputum  it  is  important  to  keep  in  mind  that  acid-fast 
streptothrix  organisms  not  infrequently  occur  in  bronchiectasis.     To  the 


DISEASES    OF   THE   BRONCHI  285 

inexperienced  these  organisms  could  be  mistaken  very  readily  for  tubercle 
bacilli.  In  a  case  under  observation  at  the  Phipps  Institute,  my  colleague, 
Paul  Lewis,  found  that  the  sputum  contained  a  streptothrix  which 
in  the  size  of  the  individual  organism  closely  resembled  the  tubercle 
bacillus.  Instead  of  being  clumped,  however,  the  organisms  were  ar- 
ranged in  long  chains  and  interlacing  filaments.  They  resisted  a  20  per 
cent,  sulphuric  acid  solution  but  were  readily  decolorized  with  30  per  cent, 
nitric  acid.  Guinea-pigs  inoculated  with  the  sputum  failed  to  develop 
tuberculosis.  When  both  tuberculosis  and  bronchiectasis  coexist  it  is 
often  impossible  to  recognize  the  presence  of  dilated  bronchi.  They  are 
to  be  suspected  if  extreme  clubbing  of  the  fingers  is  present  and  if  in  addi- 
tion, there  are  signs  of  a  cavity  in  the  area  about  the  angle  of  the  scapula. 
Tuberculosis  alone  does  not  produce  extreme  clubbing  of  the  fingers.  The 
history  of  the  case  will  also  indicate  in  some  instances,  that  the  bron- 
chiectasis antedates  the  tuberculous  infection. 

Abscess  of  the  Lung. — In  abscess  of  the  lung  the  characteristic  feature 
is  the  sudden  expectoration  of  a  large  quantity  of  mucopurulent  material, 
often  of  a  sweetish  odor.  In  the  majority  of  cases  of  abscess  the  patient 
is  acutely  ill  or  has  recently  recovered  from  an  acute  illness.  In  bronchi- 
ectasis the  development  of  the  disease  is  gradual  and  not  sudden  as  in 
abscess.  In  the  case  of  a  small  chronic  abscess  the  distinction  is  difficult. 
An  X-ray  examination  may  be  of  service.  In  case  of  doubt  an  explora- 
tory operation  should  be  advised  as  an  abscess,  if  present,  can  be  cured 
if  proper  drainage  is  secured. 

Loculated  Empyema. — At  times  an  encysted  empyema,  especially  when 
situated  between  the  lobes  of  the  lung,  ruptures  into  a  bronchus.  Under 
these  circumstances  it  is  essentially  the  same  as  a  pulmonary  abscess. 

Gangrene  of  the  Lung. — Pulmonary  gangrene  is  usually  sudden  in  onset 
and  may  be  one  of  the  sequels  of  a  pulmonary  infarct,  croupous  or  bron- 
cho-pneumonia or  tuberculosis.  If  gangrene  of  the  lung  occurs  in  an 
individual  with  a  history  of  long  standing  bronchitis  it  may  be  very  diffi- 
cult to  distinguish  it  from  bronchiectasis  with  gangrenous  changes  in 
the  bronchi.  The  presence  of  elastic  tissue  in  the  sputum  would  be  in 
favor  of  pulmonary  gangrene. 

Chronic  Bronchitis. — As  a  rule  the  presence  of  dilated  bronchi  in  a 
case  suffering  from  chronic  bronchitis  can  only  be  surmised.  It  should 
be  suspected  if  there  is  marked  clubbing  of  the  fingers  and  there  is  in  addi- 
tion the  expectoration  of  thin,  mucopurulent  material  with  a  fetid  odor. 
There  may  also  be  signs  indicative  of  a  cavity  especially  in  the  lower  lobes 
of  the  lungs. 

Fetid  or  Putrid  Bronchitis 

In  those  cases  in  which  bronchiectasis,  gangrene,  or  cavities  contain- 
ing a  fetid  secretion  can  be  excluded  and  in  which  there  are  the  physical 
signs  of  bronchitis,  it  has  been  customary  to  designate  the  condition  as 
fetid  or  putrid  bronchitis.  The  affection  is  in  reality  a  form  of  bron- 
chiectasis. In  such  cases  the  dilatation  of  the  bronchi  is  not  sufficiently 
marked  to  give  the  physical  signs  commonly  associated  with  bronchi- 
ectasis. Since  the  introduction  of  the  X-rays,  however,  it  has  become 
apparent  that  cases  which  in  former  times,  would  have  been  classed 
as  fetid  bronchitis  are  in  reality  examples  of  bronchiectasis.  By  means 
of   stereoscopic    plates  small  dilatations  of  the  bronchi  can  be  shown. 


286      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

Aside  from  the  physical  signs  the  clinical  features  of  fetid  bronchitis 
are  essentially  the  same  as  those  occurring  as  the  result  of  well-marked 
dilatation  of  the  bronchi.  The  cough  may  be  paroxysmal  in  charac- 
ter and  followed  by  the  expectoration  of  a  foul  smelling  sputum.  The 
expectorated  matter  is  usually  thin,  grayish-white  in  color  and  on 
standing  separates  into  three  layers :  the  upper  layer  is  frothy  and  often 
of  a  greenish  color,  the  middle  layer  is  serous  in  character  and  slightly 
cloudy  and  the  third  layer  consists  of  a  sediment  in  which  may  sometimes 
be  found  small  dirty  yellow  masses  known  as  Dittrich's  plugs.  As  in 
the  case  of  true  bronchiectasis  abscess  of  the  brain  is  not  an  uncommon 
terminal  event. 

Bronchiolectasis 

This  term  is  applied  to  a  form  of  bronchiectasis  in  which  the  patho- 
logical changes  are  limited  to  the  bronchioles.  Although  this  type  of 
the  disease  was  described  many  years  ago  by  Carr,1  of  England,  it  has 
been  almost  entirely  overlooked  in  this  country. 

Etiology. — The  condition  is  not  common  and  occurs  almost  exclusively 
in  young  children  who  are  poorly  nourished,  syphilitic  or  rachitic.  The 
exciting  cause  is  generally  some  one  of  the  acute  infections  such  as  whoop- 
ing cough,  measles,  diphtheria,  etc.  Bronchiolectasis  is,  as  a  rule,  an 
acute  affection. 

Morbid  Anatomy. — The  condition  is  bilateral  and  may  involve  a 
large  part  or  even  all  of  both  lungs.  The  lungs  are  usually  bulky  and 
scattered  over  the  surface  there  may  be  a  number  of  small  transparent 
bladder-like  elevations  which  correspond  to  the  small  cavities  within  the 
lungs.  On  section  the  lungs  present  a  worm-eaten  or  honeycombed 
appearance  due  to  the  numerous  small  cavities.  The  cavities  are  small, 
the  largest  about  the  size  of  a  pea,  have  smooth  walls  and  contain  either 
air  or  a  frothy  mucus.  The  bronchi  are  unaffected.  In  addition  to  the 
dilatation  of  the  bronchioles  there  is  usually  present  a  peribronchial  in- 
flammation, patches  of  broncho-pneumonia  and  some  compensatory 
emphysema. 

Occasionally  a  chronic  form  of  the  disease  occurs.  In  such  cases 
chronic  interstitial  changes  take  place  in  the  pulmonary  tissue  surround- 
ing the  dilated  bronchioles.  This  leads  to  fibrosis  of  the  affected  parts 
with  retraction  of  the  lung. 

Symptoms. — Cough  is  the  most  prominent  symptom  and  as  the 
disease  advances  tends  to  become  paroxysmal.  It  may  resemble  whoop- 
ing cough.  In  very  young  children  there  may  be  no  expectoration  as  it 
is  swallowed,  but  if  the  child  vomits,  pus  may  be  mixed  with  the  stomach 
contents.  Fever  may  be  absent  but  with  the  successive  development  of 
patches  of  broncho-pneumonia  the  temperature  often  rises  to  103°  or 
104°F. 

Anemia  and  emaciation  are  usually  marked  features  in  children  who 
develop  this  condition. 

As  a  rule  the  disease  is  acute  and  death  may  occur  as  early  as  two 
weeks  from  the  onset.  In  some  instances  it  becomes  chronic  and  may 
exist  for  three  or  four  years  or  longer. 

Physical  Signs. — In  the  chronic  cases  marked  clubbing  of  the  fingers 
may  be  noted.  As  the  disease  is  bilateral  in  most  instances  there  is  no 
1  Practitioner,  1891,  vol.  xlvi ,  p.  87. 


DISEASES    OF   THE   BRONCHI  287 

noticeable  difference  in  the  two  sides.  Scattered  rales  throughout  both 
lungs  may  be  heard  and  they  may  be  of  all  varieties.  If  they  have  a 
ringing  metallic  quality  they  are  very  suggestive  of  cavities.  The 
percussion  note  and  breath  sounds  may  show  little  if  any  abnormality. 
If  the  process  is  more  or  less  localized  in  one  or  both  lower  lobes  the 
percussion  note  may  be  impaired  or  it  may  have  a  tympanitic  quality. 
Under  these  circumstances  the  breath  sounds  may  be  suppressed,  broncho- 
vesicular  or  even  bronchial,  depending  somewhat  on  the  presence  of  an 
associated  pneumonic  process. 

Diagnosis. — Acute  tuberculosis  is  the  condition  most  likely  to  be 
confused  with  bronchiolectasis.  The  physical  signs  in  both  conditions 
may  simulate  each  other  closely.  Fowler  has  pointed  out  that  in  bron- 
chiolectasis the  general  symptoms  are  not  nearly  so  severe  as  one  would 
expect  from  the  physical  signs  and  that  improvement  of  the  child  may  be 
noted  while  the  evidences  of  pulmonary  damage  are  increasing. 

In  acute  tuberculosis  fever  is  nearly  always  a  marked  feature,  and 
emaciation  is  progressive  and  marked.  If  sputum  cannot  be  obtained 
the  pus  in  the  vomited  matter  should  be  examined  for  tubercle  bacilli. 

FOREIGN  BODIES  IN  THE  AIR   PASSAGES 

The  aspiration  of  a  foreign  body  into  the  air  passages  is  now  recog- 
nized as  a  relatively  common  accident.  And  while  the  number  of  in- 
stances reported  in  the  literature  is  in  the  aggregate  fairly  large,  the 
opportunity  of  seeing  many  of  these  cases  does  not  often  fall  to  the  lot 
of  individual  observers.  The  first  detailed  study  of  the  results  of  foreign 
bodies  lodging  in  the  air  passages  was  that  made  by  Stokes.1  In  1854 
Gross2  contributed  a  monograph  on  the  subject.  Since  that  time  there 
have  been  a  number  of  contributions.  In  1909  Eicken3  reported  303 
cases  in  which  the  bronchoscope  had  been  used  to  extract  a  foreign  body. 
The  most  comprehensive  presentation  of  the  subject  in  American  litera- 
ture has  been  made  by  Chevalier  Jackson.4 

Etiology. — A  great  variety  of  articles  may  gain  entrance  into  the 
air  passages.  The  object  may  be  one  normally  taken  into  the  mouth, 
such  as  an  article  of  food;  or  it  may  be  one  held  in  the  mouth  for  con- 
venience, such  as  a  pin;  or,  as  in  the  case  of  small  children,  toys  or  other 
small  objects  may  be  placed  in  the  mouth.  The  aspiration  of  the  foreign 
body  usually  follows  some  sudden  and  unexpected  inspiratory  effort 
such  as  may  accompany  coughing,  laughing,  a  fright  or  a  blow  on  the 
back.  Under  these  circumstances  the  foreign  body  may  enter  the  larynx 
during  "what  may  be  termed  a  moment  of  surprise  on  the  part  of  the 
epiglottis  while  raised  in  the  act  of  a  sudden  deep  inspiration."  In 
other  instances,  insensibility  of  the  upper  air  passages  as  the  result  of 
sleep,  narcosis  or  coma  may  permit  the  entrance  of  a  foreign  body.  Occa- 
sionally a  foreign  body,  in  the  form  of  food,  enters  the  larynx  during  the 
act  of  vomiting. 

In  about  one-half  of  the  cases  recorded  the  victims  of  this  accident 
have  been  children.  This  is  to  be  explained  by  the  fact  that  small 
children  have  a  habit  of  placing  all  sorts  of  objects  in  their  mouths. 

1  "Diseases  of  the  Chest,"  New  Sydenham  Society. 

2  "Foreign  Bodies  in  the  Air  Passages." 

3  Deut.  Klinik,  vol.  xii,  1909. 

4  "Peroral  Endoscopy  and  Laryngeal  Surgery,"  1915. 


288      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

Any  article  capable  of  passing  the  glottis  may  be  drawn  into  the 
larynx  during  a  forced  inspiration.  Among  the  commoner  objects  may 
be  mentioned  needles,  pins  of  various  kinds,  tacks,  pieces  of  meat,  beans 
and  fragments  of  bones.  In  one  case  observed  by  us  an  extracted  tooth 
entered  the  larynx  during  nitrous  oxide  anesthesia. 

Morbid  Anatomy. — Complete  blocking  of  the  laryngeal  opening  by 
a  foreign  body  is  fortunately  not  common,  although  such  accidents 
do  occur  and  may  be  followed  by  death  within  a  few  minutes.  In  such 
cases  a  large  piece  of  meat  is  the  most  common  offender. 


Fig.  225. — Trachea  and  bronchi  viewed  from  behind.  Note  the  larger  size  of  the  right 
bronchus  and  its  straighter  course.  The  nail  shown  in  the  glass  tube  had  lodged  in  the 
right  bronchus  at  A  where  it  ulcerated  through  into  the  lung.  {Jefferson  Medical  College 
Museum.) 


Having  passed  the  glottis  the  foreign  body  may  lodge  in  one  of  the 
ventricles  of  the  larynx.  In  the  majority  of  instances  the  object  passes 
down  the  trachea  and  in  about  80  per  cent,  of  the  cases  enters  the  right 
bronchus.  The  greater  liability  of  the  right  side  is  due  to  the  fact  that 
the  right  primary  bronchus  is  larger  and  straighter  than  the  left  (see 
Figs.  225  and  226).  The  passage  downward  of  the  foreign  body  is 
facilitated  by  gravity  and  by  the  inspiratory  widening  of  the  trachea  and 
main  bronchi.  The  rapidity  with  which  the  foreign  substance  passes 
downward  is  due  in  part  to  its  size  and  in  part  to  the  shape  of  the  object. 
In  any  case  there  is  produced  irritation  and  spasm  of  the  larynx  and 
trachea  and  more  or  less  severe  paroxysms  of  coughing  in  the  effort  to 
dislodge  the  object.     As  a  rule  the  severity  of  the  symptoms  subside  with 


DISEASES    OF    THE    BRONCHI 


289 


the  final  lodgment  of  the  foreign  body  in  one  of  the  larger  branches  of  the 
bronchial  tree. 

Spontaneous  expulsion  of  the  foreign  substance  may  occur  at  an 
early  period  or  months  or  years  may  elapse.  In  one  case  under  my  care 
a  tooth  was  coughed  up  eighteen  months  after  it  had  aspirated  into  the 
bronchi;  in  another  case  a  brass-headed  tack  was  expelled  four  or  five 
years  after  it  had  entered  the  bronchus.  In  124  cases  recorded  by  Dur- 
ham in  which  recovery  followed  spontaneous  expulsion,  the  interval  in  28 
of  the  cases  was  from  one  to  seventeen  years.  Jackson  has  reported 
cases  in  which  the  foreign  body  was  removed  some  years  after  the  initial 
accident ;  in  one  case  an  interval  of  twenty-six  years  had  elapsed. 


Fig.' 226. — Xo.  14914  (Phipps  Institute).  Child  age  six.  Cough,  3  years.  Physical 
signs  of  a  chronic  inflammatory  condition  at  right  base.  Onset  of  symptoms  indefinite. 
X-ray  showed  fibrosis  of  lung  and  dilated  bronchi,  due  to  a  bent  hatpin  measuring  2Yi 
inches  in  length  with  the  head  down  and  the  point  up. 

Spontaneous  expulsion  will  depend  on  the  nature  of  the  foreign  body. 
If  it  is  small  and  devoid  of  sharp  points  it  may  be  coughed  up  but  if  it 
is  long,  narrow  and  sharp-pointed,  such  as  a  hair  pin  or  a  safety  pin,  the 
only  hope  of  relieving  the  patient  lies  in  surgical  interference  or  the  use 
of  the  bronchoscope. 

If  the  foreign  substance  remains  in  the  larynx  edema  may  develop 
later.  The  end  results  of  lodgment  in  one  of  the  bronchi  are  varied. 
The  first  change  is  simple  inflammatory  swelling-of  the  mucous  membrane. 
If  the  substance  remains  the  inflammation  persists,  eventually  becoming 
chronic  and  with  it  there  is  apt  to  be  some  ulceration.  As  bacteria^  are 
commonly  carried  by  the  foreign  body  infection  occurs  and  this  may 

19 


290      DISEASES   OF   THE  BRONCHI,    LUNGS,    PLEURA,   AND  DIAPHRAGM 

rupture  through  the  bronchus  giving  rise  to  a  localized  abscess.  In 
addition  there  is  usually  more  or  less  of  an  inflammatory  change  or  abscess 
formation  in  the  surrounding  pulmonary  tissue.  This  eventually  becomes 
chronic  and  gives  rise  to  fibrosis  with  or  without  dilatation  of  the  bronchi 
in  the  affected  portion.  Partly  as  the  result  of  inflammatory  changes 
which  swell  the  mucous  membrane  and  partly  as  the  result  of  the  foreign 
body  itself  the  bronchus  is  obstructed,  ending  in  an  abscess  below  the 
foreign  body.  Later  sloughing  or  ulceration  follows  in  the  tissues  sur- 
rounding the  foreign  body  and  permitting  the  slow  escape  of  the  pus. 
The  bronchial  wall  may  be  destroyed  by  ulceration  and  chondrial 
necrosis.  In  some  cases  the  foreign  body  may  fall  to  the  bottom  of  the 
abscess  cavity  or  as  the  result  of  being  firmly  imbedded  it  may  remain 
fixed  in  its  original  place.  Although  the  bronchial  stenosis  is  usually 
followed  by  dilatation  of  the  bronchi  below  the  point  of  obstruction  the 
air  passages  may  remain  normal  in  size  although  filled  with  pus.  The 
term  "drowned  lung"  has  been  suggested  for  this  condition.  Later,  if 
the  obstruction  is  not  removed,  a  true  bronchiectasis  may  develop. 
In  the  case  of  a  rounded  object  complete  occlusion  of  a  bronchus  may 
occur  with  collapse  of  the  lung  tissue  to  which  the  bronchus  is  dis- 
tributed. In  some  instances  a  fibrinous  or  serofibrinous  pleurisy  occurs. 
Rarely  the  visceral  layer  of  the  pleura  is  perforated  and  an  empyma  or 
pneumothorax  develops. 

Broncho-pneumonia  or  lobar  pneumonia  sometimes  develops  within 
a  few  days  of  the  aspiration  of  a  foreign  body.  If  the  foreign  substance 
consists  of  a  bolus  of  food  and  the  particles  enter  the  finer  bronchi  a 
septic  bronchopneumonia  is  almost  certain  to  occur. 

Symptoms. — The  symptoms  produced  by  the  aspiration  of  a  foreign 
body  into  the  air  passages  may  be  divided  into  primary  and  secondary 
manifestations,  between  which  a  period  of  comparative  latency  may 
intervene. 

Immediately  following  the  entrance  of  the  foreign  body  into  the 
larynx  the  patient  is  seized  with  a  paroxysm  of  coughing,  becomes 
dyspnoic  and  cyanosed.  In  most  instances  the  patient  experiences  the 
sensation  of  suffocation.  If  the  body  is  large  the  patient  may  present 
the  appearance  of  one  strangling  to  death.  The  eyes  protrude,  the 
face  becomes  livid,  and  there  may  be  vomiting,  convulsions  and  finally 
loss  of  consciousness.  Death  may  occur  within  a  few  minutes — but 
fortunately  this  accident  is  relativehT  rare.  The  violence  of  the  initial 
symptoms  may  last  from  a  few  minutes  to  an  hour  or  more  and  may 
recur  at  intervals. 

Succeeding  the  acute  symptoms  there  may  be  some  hoarseness  if  the 
vocal  cords  have  been  injured  or  the  foreign  body  remains  in  the  larynx. 
There  may  be  a  sense  of  soreness  beneath  the  sternum  and  very  often 
the  tenderness  is  referred  to  the  right  of  the  sternum.  Expectoration, 
if  present,  is  scanty  and  may  be  blood-tinged.  Dyspnea  and  cough  may 
persist,  recur  in  paroxysms  or  entirely  disappear  for  a  time. 

Price1  in  reporting  30  cases  from  Chevalier  Jackson's  clinic  states  that 
the  immediate  effect  produced  by  the  foreign  body  was  choking  spells  in 
21;  coughing  in  14;  dyspnea  in  14;  dyspnea  occurring  later  in  4,  cyanosis 
in  5,  spasmodic  cough  in  4,  bloody  expectoration  in  5,  inspiratory  crow- 
ing in  2  and  aphonia  in  1.  Jackson  emphasizes  the  importance  of  these 
1  Penna.  Med.  Jour.,  December,  1915. 


DISEASES    OF   THE   BRONCHI  291 

initial  symptoms.  In  a  number  of  cases  observed  by  him  the  possibility 
of  a  foreign  body  being  present  had  been  ridiculed  or  ignored.  It  must 
not  be  forgotten  that  a  foreign  body  may  lodge  in  the  bronchi  without 
causing  symptoms,  even  cough,  for  an  interval  of  a  number  of  weeks 
between  the  initial  choking  and  the  vague  onset  of  bronchial  and  later, 
general  symptoms.  Thornval1  has  reported  16  cases  some  of  which 
had  no  symptoms  whatever  until  some  time  had  elapsed.  All  but  2 
of  these  cases  were  children. 

The  secondary  manifestations  develop  insidiously.  The  cough  gradu- 
ally becomes  worse  and  is  attended  with  considerable  mucopurulent 
expectoration.  In  some  cases  tuberculosis  is  suspected  because  of  the 
hectic  type  of  fever,  sweating  and  loss  of  weight.  In  others  there  is  a 
gradually  developing  fibrosis  of  the  affected  portion  of  the  lung,  dilata- 
tion of  the  bronchi  and  all  the  symptoms  of  bronchiectasis,  namely: 
a  paroxysmal  cough,  large  quantities  of  purulent  sputum,  some  fever 
and  clubbing  of  the  fingers.  The  sudden  expectoration  of  a  large  quan- 
tity of  purulent  material  may  be  the  first  intimation  of  a  pulmonary 
abscess.  Exertion  or  change  of  posture  sometimes  brings  on  a  paroxysm 
of  coughing. 

Xo  matter  what  the  particular  lesion  is,  permanent  lodgment  of  a 
foreign  body  in  the  lung  is  usually  attended  with  cough,  the  expectora- 
tion of  purulent  sputum,  some  fever  and  often  with  loss  of  weight. 

If  the  patient  is  seen  within  a  day  or  so  of  the  accident  the  upper  air 
tract  should  be  examined  with  a  laryngoscope.  If  there  is  available 
one  who  can  use  the  bronchoscope  this  method  should  also  be  utilized. 
In  all  cases  stereoscopic  X-ray  plates  of  the  chest  should  be  made. 

Physical  Signs. — There  is  nothing  distinctive  in  the  physical  signs 
which  may  be  encountered  in  cases  with  a  foreign  body  in  the  lungs. 
The  signs  are  usually  those  of  some  other  familiar  condition  such  as 
fibrosis  of  the  lung,  bronchiectasis,  abscess,  empj^ema,  or  pneumothorax. 

Diagnosis. — In  the  absence  of  any  history  of  the  accident  one  should 
always  be  alert  to  the  possibility  of  a  foreign  body  in  cases  simulating 
tuberculosis  but  in  which  the  physical  signs  are  limited  to  one  of  the 
lower  lobes.  The  same  is  true  of  bronchiectasis.  In  the  presence  of 
these  two  conditions  a  foreign  body  is  constantly  overlooked. 

In  some  instances  the  foreign  body  may  completely  block  one  of 
the  large  bronchi  and  cause  collapse  of  all  or  a  large  portion  of  a  lower 
lobe.  In  such  cases  the  absence  of  breath  sounds  and  dulness  may  lead 
to  a  diagnosis  of  fluid. 

Inasmuch  as  a  variety  of  conditions  may  be  caused  by  the  lodgment 
of  a  foreign  substance  in  the  bronchi  or  pulmonary  tissue  the  physical 
signs  give  no  direct  clue  as  to  its  presence.  The  occurrence  of  such  a 
.  possibility,  however,  is  always  to  be  borne  in  mind  when  the  signs  are 
limited  to  the  lower  lobes,  especially  the  right  lower  lobe.  We  have  made 
it  a  routine  practice  at  the  Phipps  Institute  to  have  an  X-ray  examina- 
tion made  in  all  cases  of  this  nature  and  every  now  and  then  are  rewarded 
with  the  finding  of  a  foreign  body.  Even  if  the  X-rays  fail  to  show  a 
foreign  body,  valuable  evidence  is  often  obtained  by  the  showing  of  a 
localized  inflammatory  area  in  the  lung  which  may  suggest  the  true 
nature  of  the  trouble.  As  the  value  of  the  X-rays  is  limited  chiefly  to 
metallic  objects  the  bronchoscope  should  be  employed  whenever  possible. 
1  Ugeskrift  for  Laeger,  Dec.  23,  1915. 


292       DISEASES    OF   THE  BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

By  using  the  latter  instrument,  pieces  of  bone,  beans  or  other  articles  of 
food  may  be  discovered  which  will  often  escape  detection  in  the  X-ray 
plate.  In  the  hands  of  a  skilled  operator  bronchoscopy  isthe  method  of 
choice,  as  it  is  possible  to  directly  locate  the  foreign  body  and  at  the  same 
time  remove  it.  Price  warns  against  the  use  of  the  bronchoscope  by 
those  not  possessing  the  requisite  skill.  He  reports  three  cases  in  which 
broncho-pneumonia  followed  the  trauma  produced  by  unsuccessful 
attempts  to  use  the  instrument. 


CHAPTER  XXII 
DISEASES  OF  THE  LUNGS 

TUBERCULOSIS  OF  THE  LUNGS 

"Consumption  of  the  lungs  may  be  traced  with  certainty  in  the  writ- 
ings of  every  period  as  far  back  as  the  earliest  attempts  of  the  ancient 
world  to  deal  with  medicine  according  to  method.  History  does  not 
inform  us,  however,  of  the  extent  to  which  the  malady  had  been  prevalent 
during  former  times  in  various  parts  of  the  world  ....  But  there  can 
be  no  question  that  pulmonary  consumption  has  held  at  all  times  and 
among  all  civilized  peoples  a  foremost  place  among  the  national  diseases. 
In  our  own  age,  at  all  events,  it  occupies  one  of  the  leading  positions  in 
the  statistics  of  mortality."1 

The  above  quotation  holds  as  true  to-day  as  when  written  forty  years 
ago  and  in  spite  of  the  fact  that  the  mortality  rate  of  this  disease  has 
been  steadily  falling,  tuberculosis  must  still  be  looked  upon  as  one  of 
the  great  scourges  of  civilization.  In  this  country  it  is  the  cause  of  about 
one-tenth  of  the  deaths  annually. 

So  far  as  diseases  of  the  chest  are  concerned  a  thorough  knowledge 
of  the  various  manifestations  of  tuberculosis  is  essential.  The  term 
"protean"  is' often  applied  to  other  diseases  but  in  no  instance  is  the 
designation  more  applicable  than  in  the  case  of  tuberculosis.  In  every 
individual  who  presents  himself  with  symptoms  referable  to  the  thorax  the 
possibility  of  the  trouble  being  due  to  tuberculosis  must  always  be  considered, 
no  matter  whether  the  affection  is  acute  or  chronic. 

Not  only  is  tuberculosis  the  most  important  single  disease  the  practic- 
ing physician  has  to  deal  with  but  in  addition  it  possesses  the  greatest 
interest  to  the  sanitarian  by  reason  of  its  widespread  prevalence  among 
domestic  animals.  Tuberculosis  is  not  uncommonly  found  in  pigs,  and 
among  cattle  it  is  very  prevalent.  As  we  derive  all  of  our  milk  and  a 
large  proportion  of  our  meat  from  bovine  sources,  it  is  essential  that 
measures  be  taken  to  prevent  the  spread  of  the  disease  by  the  adequate 
inspection  of  abattoirs  and  dairy  herds  and  further,  by  the  pasteuriza- 
tion of  all  milk. 

Three  types  of  tuberculosis  of  the  lungs  are  recognized:  (1)  chronic 
pulmonary  tuberculosis;  (2)  acute  pulmonary  tuberculosis;  and  (3) 
fibroid  tuberculosis. 

CHRONIC  TUBERCULOSIS  OF  THE  LUNGS 

Chronic  pulmonary  tuberculosis  is  also  known  as  tuberculosis  of  the 
lungs,  chronic  ulcerative  tuberculosis,  phthisis  and  consumption. 

Etiology. — The  cause  of  tuberculosis  is  the  tubercle  bacillus,  the  source 
of  which  is,  in  the  vast  majority  of  cases,  the  sputum  from  human  cases 
and,  to  a  lesser  extent,  the  milk  from  tuberculous  cows. 

The  tubercle  bacillus  gains  entrance  into  the  body  in  a  number ef  ways : 
1  Hirsch's  "Handbook  of  Geographical  and  Historical  Pathology,"  1S76. 

293 


294      DISEASES   OF'  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

(1)  The  most  important  mode  of  infection  is  by  inhalation.  In  the  great 
majority  of  instances  the  infection  occurs- from  the  inhalation  of  dust  in 
which  are  carried  the  tubercle  bacilli.  Careless  habits  on  the  part  of  a 
consumptive  are  entirely  responsible  for  this.  The  sputum,  which  is 
recognized  as  the  principal  source  of  infection,  is  not  dangerous  in  the 
moist  state  and  if,  in  every  instance,  it  was  destroyed  in  this  condition, 
the  disease  practically  could  be  stamped  out.  Spitting  on  the  floor  in 
the  house  or  the  immediate  surroundings  of  the  home  or  in  working  places 
permits  of  the  sputum  becoming  dried  and  mixed  with  the  dust.  Houses 
or  working  places  which  are  dark  and  badly  ventilated  are  especially 
favorable  to  prolonging  the  life  of  the  tubercle  bacillus  which  quickly 
succumbs  when  exposed  to  the  light  and  air. 

Fliigge  advanced  the  theory  that  the  chief  source  of  infection  was 
through  the  minute  droplets  which  are  expelled  during  coughing.  These 
he  believed  are  inhaled.  While  they  may,  in  some  instances,  play  a  part, 
it  is  now  generally  accepted  that  the  inhalation  of  infected  dust  is  the 
chief  source  of  the  disease  in  adults. 

In  most  instances  exposure  to  the  disease  must  be  prolonged  and  under 
the  conditions  mentioned  above.  There  is  no  danger  from  the  expired 
breath  of  consumptives  nor  from  associating  with  those  who  are  careful 
in  their  habits.  For  this  reason  a  tuberculosis  sanatorium  is  probably 
the  safest  place  one  can  be  so  far  as  the  danger  of  infection  is  concerned. 
Statistics  dealing  with  those  who  have  been  employed  for  years  in  tuber- 
culosis sanatoria  show  that  infection  practically  never  occurs  among 
these  workers. 

Until  the  study  of  marital  infeciion  by  Pope  and  Pearson1  appeared 
it  was  generally  believed  that  the  infection  of  a  wife  by  her  husband 
or  vice  versa,  was  very  common.  These  observers  from  an  analysis 
of  a  large  number  of  cases,  concluded  that  while  there  was  some  slight 
danger  from  this  source  the  majority  of  such  instances  could  be  ascribed 
to  infection  from  other  sources,  to  the  presence  of  the  necessary  diathesis 
and  to  assortive  mating. 

2  For  some  years  there  was  a  tendency  to  minimize  the  danger  from 
inhalation  and  place  infection  by  ingestion  in  the  first  place.  Infection 
through  the  digestive  tract  undoubtedly  plays  an  important  part  but 
not  to  the  extent  once  believed.  The  point  of  entrance  may  be  through 
the  tonsils  or  the  intestinal  mucous  membrane.  The  tonsillar  and  in- 
testinal routes  are  more  common  in  childhood  than  adult  life.  In  young 
children  the  intestinal  mucous  membrane  seems  to  be  especially  per- 
meable and  many  children  are  known  to  become  infected  by  being  fed 
milk  containing  bovine  tubercle  bacilli. 

3.  Localized  infection  may  occur  in  those  who  perform  autopsies, 
in  butchers,  in  handlers  of  hides,  or  in  those  who  handle  clothing  or 
utensils  used  by  consumptives.  As  a  rule  the  infection  takes  the  form 
of  a  small,  localized,  reddened,  granulation  mass  on  the  fingers  or  hand. 
Occasionally  the  infection  may  not  appear  at  the  point  of  inoculation 
but  is  carried  to  the  group  of  lymph  nodes  in  the  axilla. 

4.  The  rarest  mode  of  infection  is  the  direct  transmission  of  the 
disease  from  the  mother  to  the  fetus.  This  is  so  unusual  as  to  be 
negligible. 

Theobald  Smith    has  pointed  out   that  though  a  strictly  bacterial 
1  "Marital  Infection,"  Draper's  Company  Research  Memoirs,   190S. 


DISEASES    OF   THE    LUNGS  295 

disease  and  introduced  into  the  body  by  the  tubercle  bacillus,  which  is 
always  derived  from  some  preexisting  case  of  the  disease,  tuberculosis 
differs,  nevertheless,  from  most  diseases  in  many  important  particulars. 
Its  unknown  beginnings  in  the  body  and  its  insidious  march  after  it  has 
once  gained  a  foothold  are  responsible  for  the  existence  of  a  large  number 
of  cases  in  all  stages  of  the  disease.  In  the  earlier  stages,  while  the  dis- 
ease is  still  restricted  to  a  single  focus,  the  individual  is  to  all  outward 
appearances  in  perfect  health.  The  disease  may  remain  in  this  quiescent 
stage  indefinitely  and  then  for  one  reason  or  another  become  active.  If 
the  generally  accredited  theory  be  accepted,  namely,  that  an  initial 
implantation  takes  place  early  in  life  in  the  majority  of  people,  what  is 
it  that  determines  that  one  individual  will  later  in  life  become  tuberculous 
while  another  escapes?  The  following  factors  must  be  taken  into 
account: 

1.  We  have  to  consider  the  question  of  resistance.  Were  it  not  for 
the  fact  that  the  great  majority  of  people  possess  an  immunity  to  tubercu- 
losis the  death  rate  would  far  exceed  what  it  is  at  present.  The  degree 
of  immunity  possessed  by  the  particular  individual  varies  greatly.  In 
many  it  is  probably  absolute;  in  many  more  the  susceptibility  to  the 
infection  is  very  marked  and  they  readily  fall  victims  to  the  disease. 
The  great  majority  of  people,  in  all  probability,  possess  sufficient  resis- 
tance to  the  growth  of  the  tubercle  bacillus  providing  this  resistance 
is  not  lowered  by  other  causes. 

Another  factor  which  must  be  considered  is  the  degree  of  virulence 
of  the  tubercle  bacillus.  It  is  well  known  that  different  strains  of  the 
organism  vary  tremendously  in  virulence;  some  possess  very  little  power 
for  mischief  while  others  are  capable  of  producing  very  destructive 
lesions.  While  we  lack  sufficient  proof  as  to  the  effect  of  a  strain  of 
known  virulence,  it  is  not  unreasonable  to  assume  that  when  the  disease 
progresses  but  slowly  and  extends  over  a  period  of  years,  the  resistance 
of  the  individual  is  marked  and  that  in  addition  the  virulence  of  this 
particular  strain  is  not  great.  On  the  other  hand  rapidly  progressing 
cases  probably  represent  instances  in  which  the  resistance  is  slight  and 
the  virulence  of  the  organism  is  marked. 

That  the  white  races  have  acquired  a  certain  degree  of  immunity 
during  the  centuries  to  which  they  have  been  exposed  to  the  disease  is 
consistent  with  what  we  know  of  other  infectious  diseases.  Two  races, 
which  in  their  primitive  state  were  free  from  tuberculosis,  have  paid  a 
heavy  toll  through  association  with  the  white  race.  The  North  American 
Indian  has  been  especially  susceptible,  tuberculosis  being  one  of  the 
most  potent  causes  of  the  rapid  decimation  of  this  race.  For  the  year 
1915  the  greatest  single  cause  of  death  among  the  Indians  was  tuberculosis 
which  was  responsible  for  35.08  per  cent,  of  all  deaths.  The  negro  is 
another  example  of  a  race  which  has  been  exposed  to  the  disease  but  a 
short,  period  and  in  which  sufficient  time  has  not  elapsed  to  establish 
much  immunity.  Not  only  is  the  negro  extremely  susceptible  but,  as 
a  rule,  the  disease  pursues  a  much  more  acute  course  than  in  the  white 
man.  The  death  rate  from  tuberculosis  among  negroes  is  from  three 
and  a  half  to  four  times  that  of  the  whites.- 

2.  Heredity. — Until  comparatively  recently  it  was  taught  that 
tuberculosis  was  an  inherited  disease.  The  basis  for  this  belief  lay  in 
the  fact  that  it  was  a  common  observation  that  the  children  of  tuberculous 


296        DISEASES  OF  THE  BRONCHI,   LUNGS,   PLEURA,   AND  DIAPHRAGM 

parents  very  frequently  developed  the  disease.  We  now  know  that 
direct  inheritance  of  the  disease  is  extremely  rare,  so  much  so  as  to  be 
practically  negligible.  The  real  cause  of  tuberculosis  being  a  family 
affection  is  due  to  its  transmission  from  the  infected  parent  to  the  child 
after  birth.  This  may  occur  as  the  result  of  the  careless  disposal  of  the 
sputum  in  the  home;  by  kissing;  or  by  infection  of  the  child's  food. 
Owing  to  the  more  intimate  contact  between  the  mother  and  the  child 
it  is  well  recognized  that  a  tuberculous  mother  is  more  dangerous  to  her 
children  than  a  tuberculous  father. 

Although  a  child  is  rarely  born  tuberculous,  there  is  reason  to  believe 
that,  in  some  instances,  the  children  of  tuberculous  parents  are  more 
susceptible  than  others  and  that  when  exposed  to  infection  they  offer 
little  resistance.  Karl  Pearson,  especially,  has  been  insistent  on  the 
importance  of  a  tuberculous  diathesis. 

3.  Reinfection. — As  already  stated  many  authorities  place  the  time 
of  infection  during  the  early  years  of  life,  the  belief  being  that  the  bacilli 
lie  dormant  until  some  time  later  when,  for  one  reason  or  another,  the 
individual's  resistance  becomes  lowered  and  the  disease  becomes  active. 
An  individual  may,  however,  become  reinfected  in  adult  life  and  succumb 
to  this  second  implantation  of  the  tubercle  bacilli.  Paul  Lewis1  is  of 
the  belief  that  the  primary  infection  in  early  life  has  little  influence  on 
the  disease  as  it  presents  itself  in  adults.  This  judgment  is  based  on  his 
experience  with  bovine  vaccination  where  the  immunity  seems  not  to 
persist  much  longer  than  do  living  bacilli  introduced  as  a  preventive. 
Applied  to  the  human  type  of  the  disease  this  fact  may  be  interpreted 
as  follows :  There  is  a  high  incidence  of  infection  in  early  childhood,  very 
possibly  owing  to  an  especial  permeability  of  the  intestinal  mucous  mem- 
branes in  that  period.  By  the  adolescent  period,  however,  most  of  the 
infected  children  are  either  cured  of  the  disease  or  have  died  of  it.  Fol- 
lowing the  twentieth  year  a  fresh  period  of  high  incidence  occurs,  prob- 
ably owing  in  part  to  the  failing  natural  immunity  of  the  lungs  and  in 
part  to  increased  exposure.  There  can  be  no  doubt  that  infection  in 
adult  life  is  far  more  frequent  than  is  ordinarily  taught.  This  is  apparent 
from  the  fact  that  healthy  adults,  with  no  history  of  tuberculosis  in  the 
family,  not  infrequently  acquire  the  disease  by  moving  into  a  house 
infected  by  a  former  tenant. 

4.  Insanitary  Surroundings. — For  years  it  has  been  recognized  that 
tuberculosis  is  essentially  a  house  disease.  It  is  in  the  home,  in  the 
vast  majority  of  instances,  that  the  disease  is  acquired  and  here  from  its 
inception  to  its  close  the  entire  drama  is  played.  The  worse  the  living 
conditions  are,  the  higher  will  be  the  incidence  of  tuberculosis,  and  this 
applies  to  the  isolated  country  house  as  well  as  the  congested  city  slum. 
In  considering  the  influence  of  the  home  surroundings,  two  factors  must 
be  taken  into  account:  first,  the  home  itself;  and  secondly,  the  habits 
of  the  people. 

Much  emphasis  has  been  placed  on  the  badly  ventilated  and  lighted 
house  as  a  predisposing  cause  of  the  disease,  and  of  this  there  can  be  no 
doubt.  Another  factor,  and  one  which  is  not  so  well  recognized,  is  the 
unhygienic  habits  of  the  people  themselves.  In  a  study  made  by  the 
Phipps  Institute2  it  was  found  that  many  houses  which  had  little  to  com- 

1  Journal  of  the  Outdoor  Life,  February,  1916. 
2     Eleventh' Report,  1915. 


DISEASES    OF    THE    LUNGS  297 

mend  them  were  inhabited  by  people  who  were  cleanly  in  their  habits; 
on  the  other  hand,  model  houses  were  often  found  to  be  tenanted  by 
people  who  made  no  pretense  of  observing  the  simplest  rules  of  hygiene. 
Perhaps  the  greatest  lesson  which  the  crusade  against  tuberculosis  has 
taught  is  the  importance  of  hygiene.  Not  only  must  better  houses  be 
provided  but  in  addition  the  people  themselves  must  be  impressed  with 
the  dangers  of  insanitary  habits.  They,  must  be  taught  that  irregular 
meals,  food  of  poor  quality,  insufficient  sleep  and  dissipation  in  any  form 
lead  to  a  lowering  of  the  resistance  and  thus  render  the  individual  more 
susceptible  to  infection.  In  an  occupational  study  made  at  the  Phipps 
Institute1  it  was  shown  that  among  those  workers  who  took  their  meals 
irregularly,  and  among  those  who  did  not  get  sufficient  sleep  the  incidence 
of  tuberculosis  was  much  higher  than  in  the  case  of  those  leading  a  regular 
life. 

In  regard  to  the  influence  of  insanitary  dwellings  the  experience  of 
Liverpool  is  instructive.  The  municipal  government  tore  down  large 
sections  of  defective  dwellings  and  erected  in  their  place  sanitary  houses. 
The  same  people  were  housed  in  the  new  dwellings  who  had  occupied 
the  old  ones.  In  this  reconstructed  district  the  death  rate  from  tuber- 
culosis fell  from  4  per  1000  to  1.9  per  1000.  A  very  striking  example  of 
the  effect  of  destroying  a  slum  district  was  noted  after  the  great  fire  in 
San  Francisco.  Prior  to  the  fire  in  1905  the  death  rate  from  tuberculosis 
in  that  city  was  274  per  100,000;  two  years  later  it  had  fallen  to  179  per 
100,000.     In  1912  it  had  fallen  still  farther  to  153  per  100,000. 

Poverty  and  tuberculosis  go  hand  in  hand.  This  is  due  to  the  fact 
that  lack  of  money  forces  the  very  poor  into  the  most  insanitary  districts 
and  in  addition  does  not  permit  of  their  obtaining  suitable  food.  Both 
of  these  factors  lower  the  resistance  and  make  the  individual  a  ready 
victim  of  the  disease. 

5.  Occupation. — The  influence  of  occupation  as  a  predisposing  cause 
of  tuberculosis  has  been  emphasized  over  and  over  again.  There  are 
many  employments  which  are  credited  with  being  bad,  but  which  in 
reality  are  not,  much  of  the  evil  that  is  associated  with  them  being  the 
result  of  contributory  factors  which  are  not  directly  connected  with  the 
work  itself.  It  is  well  to  remember  that  in  the  badly  ventilated  state  of 
one  factory  compared  with  another,  the  home  life  and  surroundings  of 
the  work  people,  poverty,  heredity,  age  and  sex  are  to  be  found  condi- 
tions that  favor  the  production  of  ill  health,  and  are  therefore,  not  to  be 
ignored.  Usually  it  is  a  gradual  deterioration  of  health  that  is  produced.2 
It  cannot  be  emphasized  too  strongly  that  it  is  impossible  to  determine  the 
effect  of  a  given  occupation  as  a  predisposing  cause  cf  tuberculosis  without 
a  knowledge  of  where  and  how  the  worker  lives. 

6.  Acute  and  Chronic  Infections. — As  the  result  of  some  acute  or 
chronic  disease  the  individual  may  be  rendered  more  susceptible  to 
reinfection  with  tuberculosis,  or  as  the  result  of  lowered  resistance,  a 
quiescent  tuberculous  lesion  may  become  active.  Acute  catarrhal  con- 
ditions of  the  upper  respiratory  tract,  measles,  whooping  cough,  etc.,  are 
not  infrequently  followed  by  tuberculosis. 

The  importance  of  damp  soil  and  damp  houses  was  emphasized  many 
years  ago  by  Henry  I.  Bowditch,  who  showed  that  such  conditions  were 

1  Eighth  Report,  1915. 

2  Oliver's    "Dangerous  Trades." 


298      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

productive  of  catarrhal  affections  of  the  respiratory  tract  and  that  they 
in  turn  predisposed  to  tuberculosis.  Sims  Woodhead  also  has  pointed  out 
that  in  pulmonary  tuberculosis  the  most  important  predisposing  cause 
appears  to  be  a  catarrh.  This  is  most  apt  to  occur  in  portions  of  the  lung 
where  expansion  and  contraction  are  weak  or  imperfect,  as  at  the  apices. 
Among  the  chronic  diseases  in  which  tuberculosis  is  often  a  terminal 
infection  may  be  mentioned  diabetes,  arterio-sclerosis  and  cirrhosis  of 
the  liver. 


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^Fig.  227. — Tuberculosis;  all  forms.  Registration  area  of  the  United  ^States.  The 
dotced  line  represents  the  number  of  deaths  for  the  disease  specified  for  different  decades 
per  10,000  persons  living  ax  corresponding  decades.  The  solid  line  represents  the  ratio  of 
deaths  from  a  particular  disease  at  different  decades  to  the  whole  number  of  deaths  at 
all  ages  from  the  same  disease.  The  broken  line  in  Chart  represents  the  ratio  of  deaths 
from  tuberculosisjat  any  decade  to  the  total  number  of  deaths  from  all  causes  at  the  corre- 
sponding decade.      {Montgomery,,  Arner.  Jour.  Med.  Sc,  Sept.,  1915.) 


7.  Pregnancy  and  the  Puerperal  Period. — Many  women  first  manifest 
evidences  of  pulmonary  tuberculosis  during  or  immediately  after  the 
termination  of  pregnancy.  When  the  disease  becomes  active  during 
pregnancy  it  is  probably  due  to  the  increased  demands  made  on  the 
woman's  vitality.  When  it  first  shows  itself  during  the  puerperal  period 
or  undergoes  an  acute  exacerbation  at  this  time,  it  is  due,  in  large  measure, 
to  the  violent  efforts  attending  the  delivery  of  the  child.  It  is  noteworthy 
that  among  women  a  very  large  number  date  the  onset  of  their  pulmonary 
trouble  from  a  pregnancy. 


DISEASES    OF   THE    LUNGS  299 

A  consideration  of  the  above  etiological  factors  makes  it  apparent 
that  over  and  above  the  implantation  of  the  tubercle  bacillus  in  the  body 
something  additional  is  needed,  in  the  vast  majority  of  cases,  to  cause 
the  individual  to  develop  clinical  tuberculosis. 

For  some  years  past  I  have  been  able  to  fix  on  the  determining 
factor  in  the  great  majority  of  private  patients.  In  one  it  has  been  ex- 
cessive mental  anxiety  over  business  affairs;  in  another  the  nursing  of 
a  relative  in  a  long  and  tedious  illness;  in  still  another,  a  period  of  over- 
work and  lack  of  sufficient  sleep.  Among  the  lower  class  the  prolonged 
exposure  to  insanitary  surroundings  and  poor  food  are  to  be  looked  upon 
as  the  most  potent  causes. 

As  already  pointed  out,  no  race  is  exempt  from  the  disease  and  it  is 
to  be  met  under  all  sorts  of  climatic  conditions.  Tuberculosis  occurs  at 
all  age  periods  but  the  chronic  ulcerative  type  affecting  the  lungs  is 
essentially  a  disease  of  adult  life.  Statistics  show  that  the  highest  in- 
cidence of  pulmonary  disease  is  between  the  twentieth  and  fortieth 
years.  Montgomery,1  however,  has  called  attention  to  the  fact  that  if 
the  death  rate  is  computed  for  the  different  age  periods  in  relation  to 
those  living,  the  disease  is  as  prevalent  among  those  of  advanced  years 
as  in  early  adult  life. 

Fig.  227  pictures  the  mortality  curve  for  all  forms  of  tuberculosis 
in  the  registration  area  of  the  United  States,  and  shows  what  has  long 
been  known,  but  is  frequently  overlooked,  that  tuberculosis  continues 
unabated  its  extensive  ravages  even  among  elderly  perons,  though  the 
absolute  number  of  deaths  from  tuberculosis  is  actually  diminishing. 
Among  those  who  have  emphasized  the  high  mortality  from  tuberculosis 
among  the  aged  are  Wilson  Fox  and  Cornet.  A  recent  pamphlet  issued 
by  the  Maryland  State  Department  of  Health  entitled  "A  Brief  Review 
of  the  Tuberculosis  Campaign,  1904-1914,"  shows  that  "in  the  white 
population  beginning  with  the  twentieth  year  of  life  all  persons  are  equally 
liable  to  death  from  tuberculosis." 

Morbid  Anatomy. — A  knowledge  of  the  pathology  of  tuberculosis  as 
it  affects  the  lungs,  is  absolutely  essential  in  order  to  gain  a  clear  concep- 
tion of  its  various  manifestations. 

In  both  its  pathological  and  clinical  aspects  the  disease  may  exhibit 
the  widest  extremes.  It  may,  on  the  one  hand,  run  an  acute  course,  the 
duration  of  which  is  measured  in  weeks  or,  on  the  other  hand,  it  may 
pursue  a  chronic  latent  course  lasting  for  years.  The  very  acute  and  the 
very  chronic  cases,  however,  form  but  a  small  proportion  of  the  total 
number.  The  overwhelming  majority  of  cases  of  pulmonary  tuberculosis 
is  comprised  of  the  type  referred  to  as  chronic  ulcerative  tuberculosis; 
more  commonly  known  as  phthisis  or  consumption.  In  this  type  of  the 
disease  the  course  is  rarely  continuous  but  is  almost  invariably  charac- 
terized by  periods  of  activity  which  are  succeeded  by  periods  of  quies- 
cence or  indeed  complete  arrest  of  the  disease,  which  may  last  for  twenty 
years  or  even  longer.  The  too  commonly  accepted  belief  that  pulmonary 
tuberculosis  has  an  average  duration  of  from  two  and  a  half  to  three 
years,  is  no  longer  tenable.  In  the  vast  majority  of  cases  the  symptoms 
which  seem  to  indicate  the  beginning  of  the  trouble,  are  in  reality  ante- 
dated by  years  by  some  symptom  or  group  of  symptoms  which  cither  have 
been  ignored  or  have  been  attributed  to  some  other  disease.  This  may 
:  Amer.  Jour.  Med.  Sc.,~  September,  1915. 


300      DISEASES   OF   THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

be  illustrated  by  the  following  case  which,  while  extreme,  is  by  no  means 
uncommon. 

A  banker,  aged  fifty-two,  came  under  observation  for  the  first  time  with 
a  laryngeal  tuberculosis  and  physical  signs  which  clearly  indicated  an 
infiltrating  process  involving  the  upper  third  of  the  left  upper  lobe.  He 
stated  that  he  had  been  perfectly  well  up  to  three  months  previously. 
His  history,  however,  showed  that  he  had  had  at  the  age  of  twenty-two 
years  several  pulmonary  hemorrhages  for  which  he  was  confined  to  bed 
for  a  few  days.  Ten  years  later  he  had  a  severe  attack  of  pleurisy  which 
laid  him  up  for  a  wTeek.  This  was  followed  by  no  ill  effects.  Here 
then  we  have  a  case  in  which  the  disease  gave  warnings  of  its  presence 
thirty  and  twenty  years  prior  to  his  becoming  definitely  tuberculous. 
During  this  long  period  his  health  was  good  and  he  finally  succumbed  to 
the  infection  because  his  resistance  became  lowered  through  overwork 
and  financial  worries  during  a  business  panic.  This  man  made  a  com- 
plete recovery  and  is  at  the  present  time  perfectly  well  (seven  years 
later) . 

A  knowledge  of  the  fact  that  this  type  of  tuberculosis  is  subject  to 
the  occurrence  of  periods  of  slight  activity  which  subside  spontaneously, 
is  of  considerable  practical  importance  as  it  indicates  that  the  disease  is 
more  or  less  latent  and  chronic  and  that  the  patient's  resistance  is  good. 
In  this  type  of  case  the  prospect  of  recovery  is,  as  a  rule,  a  great  deal  more 
promising  than  in  that  with  an  acute  onset  and  no  antecedent  history 
of  trouble. 

The  acuteness  or  chronicity  of  every  tuberculous  infection  is  to  a 
great  extent  determined  by  two  factors.  On  the  one  hand,  we  have  the 
invading  tubercle  bacilli  striving  to  multiply  and  spread  and  destroy 
tissue.  Opposed  to  this  invasion  are  the  resources  of  the  host  which 
strive  to  hold  in  check  the  invaders.  While  some  of  the  tubercle  bacilli 
may  be  destroyed  by  the  phagocytes,  the  chief  defense  against  them  lies 
in  the  formation  of  fibrous  tissue  which  surrounds  the  tubercles  and 
completely'  or  partially  arrests  the  process.  That  this  is  true  is  evident 
from  the  fact  that  the  acute  types  of  the  disease  show  little  or  no  evidence 
of  fibrous  tissue  about  the  lesions,  while  in- the  more  chronic  forms  of  the 
disease  an  extensive  overgrowth  of  fibrous  tissue  constitutes  the  chief 
characteristic  of  the  pulmonary  lesions.  In  chronic  ulcerative  phthisis, 
therefore,  the  rapidity  or  slowness  of  the  progress  of  the  disease  is  deter- 
mined, largely,  by  the  capacity  of  the  lung  to  undergo  fibroid  changes. 

Sims  Woodhead  has  described  the  initial  changes  as  follows:  The 
first  stage  is  an  apical  catarrh;  that  is,  a  congestion  of  the  blood-vessels 
of  the  mucous  membrane,  accompanied  by  a  slight  proliferation  of  the 
epithelial  cells  lining  the  air  cells  with  an  increased  pouring  out  of  fluid 
and  an  emigration  of  a  large  number  of  white  cells.  This  catarrhal 
change  is  noted  in  portions  of  the  lung  where  expansion  and  contraction 
are  weak  or  imperfect,  as  at  the  apices  in  adults  or  about  the  hilus  in 
children. 

This  breeding  ground  for  the  tubercle  bacillus  may  gradually  increase 
in  size.  If,  however,  the  tissues  are  well  nourished,  fibrous  tissue  is 
formed.  Building  up  the  resistance  of  the  patient  by  proper  treatment 
aids  in  bringing  this  about.  If  this  is  accomplished,  the  bacilli  become 
inactive  and  the  degenerative  tissue  is  partly  absorbed  and  partly  trans- 
formed into  scar  tissue.     If,   however,   the   process   does  not  become 


DISEASES    OF   THE    LUNGS  301 

arrested  at  this  point,  the  disease  spreads  beyond  its  original  focus  and  a 
considerable  area  of  tuberculous  consolidation  may  be  the  result.  The 
degenerated  or  caseous  material  may  then  become  softened  and  it  is 
during  this  stage  of  softening  that  secondary  infection  goes  on  perhaps 
most  readily. 

The  initial  deposit  as  seen  at  the  autopsy  table  in  individuals  dying 
from  other  causes  may  consist  of  a  single  small  peribronchial  focus  (see 


Fig.  228. — Solitary  peribronchial  tubercle  indicated   by   arrow.     Rest  of  lung  norma 

(Jefferson  Medical  College  Museum.) 

Fig.  228)  or  it  may  consist  of  several  areas  the  size  of  a  hazel  nut.  Such 
foci  represent  the  coalescence  of  a  small  group  of  tubercles.  From  these 
areas  the  disease  spreads  or  healing  may  take  place  (see  Fig.  229). 

In  those  instances  in  which  the  disease  gains  the  upper  hand  the 
tubercles  which  at  first  are  discrete,  coalesce  and  in  addition  spread 
beyond  their  original  boundaries.  Thus  at  the  apex  where  the  original 
deposit  occurred  the  infiltration  becomes   more  and  more  dense  and 


302      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

furthermore  the  tubercles  spread  downward  until  the  entire  lung  is 
involved  although  in  the  lower  portions  the  infiltration  is  usually  widely 
scattered. 

This  constitutes  the  second  or  moderately  advanced  stage.  Fig. 
230  shows  this  very  well.  It  will  be  noted  that  at  the  extreme  apex  the 
infiltration,  while  very  dense,  has  not  replaced  entirely  all  of  the  pulmon- 
ary tissue  so  that  some  vesicular  element  will  be  retained  in  the  respira- 
torv  sounds.     The  infiltration  becomes  less  and  less  marked  as  the  base 


Fig.  229. — Below  the  apex  are  seen  several  calcareous  nodules  surrounded  by  fibrous 
tissue.  These  represent  small  deposits  of  tubercles  which  have  become  walled  off.  It  is 
in  this  way  that  tuberculosis  is  often  healed. 

of  the  lung  is  approached.     The  lower  third  is  apparently  free  from 
disease. 

The  chief  characteristic  of  chronic  ulcerative  tuberculosis  is  the 
formation  of  cavities.  As  a  rule  a  cavity  is  an  indication  that  the  dis- 
ease has  progressed  to  the  third  or  advanced  stage  of  the  disease.  This 
is  not  invariably  true,  however.  The  original  focus  may  break  down  and 
empty  out  through  a  bronchus  and  the  disease  become  arrested  at  this 
point;  and  the  same  is  true  of  the  second  or  moderately  advanced  stage. 


DISEASES    OF   THE    LUNGS  303 

In  the  advanced  stages  of  the  disease  it  is  almost  the  rule  to  find  a 
cavity  at  one  or  both  apices  and  in  addition  smaller  cavities  may  be 
present  in  other  portions  of  the  lungs. 

The  excavation  may  be  represented  by  a  single  large  cavity  with  a 
well-defined  wall  or  it  may  present  a  honeycombed  appearance  in  which 
the  cavities  are  small  and  communicating  with  ragged  necrotic  walls. 
The  former  type  is  characteristic  of  the  chronic  type  of  the  disease,  the 
latter  of  the  more  acute  forms  (see  Acute  Pulmonary  Tuberculosis). 


Fig.  230. — Dense  infiltration  of  upper  lobe.     Areas  of  conglomerate  tubercles  in  upper 

part  of  lower  lobe. 

It  is  the  present  belief  that  the  formation  of  a  cavity  is  due  int  large 
part,  to  the  presence  of  secondary  infections  with  the  various  pus-produc- 
ing organisms.  These  organisms  produce  a  liquefying  necrosis  of  the 
caseous  areas  and  thus  hasten  their  breaking  down.  The  final  stage  in 
the  formation  of  a  cavity  is  the  rupture  of  the  caseous  and  necrotic.,  area 
into  a  bronchus.     As  a  rule  there  is  but  one  such  communication;' but 


304      DISEASES   OF   THE  BRONCHI,    LUNGS,    PEETJRA,    AND   DIAPHEAGM 

there  may  be  two  or  three,  in  which  case'  the  physical  signs  are  apt  to  be 
indefinite  and  imperfect. 

The  longer  the  tuberculous  process  lasts  the  more  certainly  is  excava- 
tion apt  to  occur  although  this  is  not  an  invariable  rule,  particularly  in 
the  chronic  fibroid  cases.  Recently  formed  cavities  have  an  irregular 
outline,  are  ill-defined,  the  interior  is  ragged  and  there  is  an  absence  of  a 
distinct  wall.  When  the  process  is  not  acute  or  has  remained  localized 
for  some  time,  a  more  or  less  well-formed  wall  of  fibrous  tissue  develops. 


Fig.  231. — Cavity  in  apex  of  right  upper  lobe  and  a  smaller  one  anteriorly  just 
beneath  the  clavicle.  In  addition  to  cavities  there  is  healthy  pulmonary  tissue  and  con- 
siderable fibrosis.      Illustrates  a  chronic  and  slowly  progressive  type  of  disease. 

The  longer  the  cavity  has  existed  the  thicker  the  fibrous  tissue  about  it. 
Furthermore,  the  caseous  lining  of  the  cavity  gradually  changes  into 
granulation  tissue  and  this  in  turn  may  be  replaced  by  smooth  fibrous 
tissue. 

Fig.  231  represents  a  chronic  type  of  infection.  The  cavity  is  sharply 
defined  and  from  its  shape  seems  to  have  been  formed  by  several  smaller 
excavations  which  have  united.  Below  the  cavity  is  a  scattered  infiltra- 
tion with  some  fibroid  changes  and  dilatation  of  the  bronchi. 


DISEASES    OF    THE    LUNGS 


305 


Fig.  232  illustrates  how  extensive  the  pulmonary  excavation  may 
become.  In  this  instance  practically  the  entire  lung  has  been  reduced 
to  a  fibrous  shell  with  only  a  fringe  of  pulmonary  tissue  at  the  base. 

Another  important  feature  of  cavities  is  that  those  of  any  considerable 
size  contain  in  their  walls  or  the  trabecula  traversing  them,  blood-vessels 
(Fig.  233).     As  a  rule  the  blood-vessels  in  and  about  the  cavity  become 


Fig.  232. 


-Case  No.  2388  (Phipps  Institute).     Upper  three-fourths  of  lung  taken  up  by 
three  cavities  with  great  outgrowth  of  fibrous  tissue. 


thrombosed  and  obliterated.  If  they  remain  patulous,  small  aneurismal 
dilatations  occur  in  their  walls  and  the  rupture  of  one  of  these  will  give 
rise  to  a  hemorrhage.  Fig.  234  represents  a  cavity  filled  with  blood  clot 
in  which  this  accident  occurred.     (See  also  Fig.  59.) 

In  addition  to  a  knowledge  of  how  the  disease  develops  it  is  important 
to^recognize  the  routes  it  follows  from  the  time  the  initial  deposit  of 
tubercles  occurs  to  the  final  stages.     The  proportion  of  cases  in  which 

20 


306 


DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 


the  apex  is  the  primary  site  of  the  disease  is  so  large  that,  generally  speak- 
ing, the  exceptions  can  be  disregarded.  Laennec's  brief  description  of 
the  successive  change  is  worth  quoting:  "We  very  often  find  in  the 
same  lung  evident  proofs  of  two  or  three  successive  eruptions,  and  we 
can  then  nearly  always  make  out  that  the  primary  eruption  at  the  apex 
of  the  lung  has  already  become  excavated;  that  the  second,  situated 
around  the  first,  but  a  little  lower,  is  formed  by  tubercles  which,  in 
most  instances,  are  already  yellow,  though  still  small;  that  the  third, 
formed  by  gray  miliary  tubercles,  with  some  yellow  points  in  the  center, 
occupy  a  still  lower  zone." 


Fig.  233. — Large  cavity  in  upper  lobe  with  blood-vessels  laid  bare. 


These  features,  namely,  the  primary  deposit  in  one  or  the  other  apex; 
the  extension  downward  and  the  presence  of  the  greatest  damage  where 
the  disease  first  began,  are  characteristic  of  tuberculosis  and  serve  as 
valuable  aids,  inasmuch  as  the  physical  signs  will  be  more  marked  at 
the  summit  of  the  lung  and  while  continuous,  diminish  as  the  base  is 
approached.  This  distribution  of  the  disease  also  serves  to  distinguish 
tuberculosis  from  certain  chronic  inflammatory  diseases  of  the  lung,  which 
invade  the  base  rather  than  the  apex.  While  these  generalizations  are 
not  absolute,  "the  line  of  march"  in  the  great  majority  of  cases  un- 
doubtedly shows  a  great  similarity. 

Not  only  are  the  apices  usually  the  original  site  of  the  disease,  but  as 
Fowler  has  shown,  a  fairly  definite  area  in  the  apex  is  the  common 


DISEASES    OF    THE    LUNGS 


307 


starting  point.  This  point  is  about  1  inch  to  l}i  inches  below  the  apex, 
and  corresponds  anteriorly  to  the  supraclavicular  fossa  or  the  middle  of 
the  clavicle.  Extending  from  this  point  the  disease  tends  to  spread 
backward.     As  the  process  spreads,  it  progresses  downward,  the  mfil- 


Fig.  234.— Right  lung.  Advanced  tuberculosis.  Several  cavities,  the  Largest,  al  the 
bottom  of  the  upper  lobe  posteriorly  is  filled  with  blood  clot.  (Patient  died  of  hemoptysis.; 
fix  tensive  infiltration  and  fibrosis  of  both  lobes. 

tration  about  the  original  focus  increasing  and  gradually  thinning  out  as 
the  base  is  reached. 

A  less  usual  site  for  the  primary  infection  occurs  at  a  point  which 
corresponds  to  the  first  and  second  interspaces  below  the  outer  third  of 
the  clavicle. 

Of  almost  equal  importance  to  the  primary  infections  m  the  apex 


•308      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

are  the  secondary  deposits  in  the  lower  lobes.  Fowler  points  out  that 
the  involvement  of  the  lower  lobe  may  be  very  early  in  the  disease  and 
that  although  it  follows  the  primary  apical  infection,  may  give  more 
definite  physical  signs  because  of  the  doubtful  character  of  the  apical 
findings.  As  a  rule  the  apex  of  the  lower  lobe  is  first  involved.  This 
corresponds  to  a  point  opposite  the  fifth  dorsal  vertebra  in  the  inter- 
scapular region  (Fig.  235).  From  this  point  the  disease  tends  to  spread 
downward  along  the  interlobar  septum,  which  is  roughly  indicated  by 
the  inner  border  of  the  scapula,  when  the  hand  is  placed  on  the  opposite 
shoulder. 


Fig.  235. — Specimen  showing  a  small  deposit  of  tubercles  in  posterior  aspect  of  right 
upper  lobe  and  in  the  apex  of  the  lower  lobe.  Corresponds  to  the  right  interscapular 
-region  opposite  fourth  and  fifth  dorsal  vertebra. 

Following  the  involvement  of  the  upper  lobe  the  disease  if  progressing, 
"manifests  itself  in  the  opposite  apex;  less  commonly,  according  to  Fowler, 
in  the  upper  lobe  at  a  point  corresponding  with  the  apex  of  the  axilla. 
Disease  of  one  apex  with  secondary  manifestations  in  the  opposite  lower 
Sobe  occasionally  occur. 

One  rarely  finds  during  the  terminal  stage  of  the  disease,  that  both 
lungs  are  equally  diseased.  The  lung  primarily  affected  is  generally 
more  extensively  involved  and  the  destruction  of  tissue,  as  manifested 
by  cavity  formation,  greater.  The  lung,  secondarily  affected,  may  be 
markedly  diseased  in  the  upper  lobe,  but  the  lower  will  be  free,  or  at  most 
contain  scattered  tubercles.  During  the  terminal  months  of  the  disease 
the  lower  part  of  one  or  the  other  lung,  which  undergoes  a  certain  amount 
of  compensatory  emphysema,  supplies  the  patient  with  most  of  his 
breathing  space  (Fig.  236;  see  also  Fig.  101). 


DISEASES    OP    THE    LUNGS  309 

Another  change,  and  one  that  probably  follows  the  pulmonary  in- 
fection very  quickly,  is  a  low-grade  inflammation  of  the  apical  pleura 
which  results  in  the  obliteration  of  the  pleural  cavity  at  that  point. 
While  the  clinical  evidence  of  this  is  not  great,  it  is  an  almost  constant 
finding  that  in  individuals  who  have  died  of  chronic  tuberculosis  the 
apices  of  the  lungs  are  firmly  adherent  to  the  chest  wall  and  that  this  is 
most  noticeable  over  the  posterior  surface. 

As  the  pulmonary  infection  spreads  the  overlying  pleural  space  be- 
comes obliterated.     Involvement  of  the  pleura  in  tuberculosis  is  always 


Fig.  236. — Viewed  from  behind.  Large  cavity  in  left  upper  lobe;  dense  infiltration 
and  fibroid  changes  in  lower  lobe.  Right  upper  lobe  densely  infiltrated  with  recently 
formed  cavities.     Right  lower  lobe  practically  free  from  disease. 

greatest  at  the  apex  where  the  trouble  originated  (Fig.  237).  At  the 
apex  the  thickening  is  dense,  gradually  thinning  out  as  the  base  of  the 
lung  is  reached.  While  often  dense  throughout  and  binding  the  entire 
lung  firmly  to  the  chest  wall,  the  adhesions  over  the  lower  part  of  the  lung 
are  more  commonly  lace-like  and  easily  broken  up.  (See  also  section  on 
Pleurisy,  p.  527.) 

Obliteration  of  the  pleural  space  is,  to  a  great  extent,  a  protective 
measure.  Were  it  not  for  this  a  pneumothorax  would  likely  oficur  in 
the  majority  of  cases  of  tuberculosis  instead   of   being  relatively    un- 


310      DISEASES   OF   THE  BEONCHI,    LUNGS,    PLETJEA,   AND   DIAPHEAGM 

common.  A  more  extended  description  of  the  changes  which  occur  in 
tuberculous  pleurisies  and  in  pneumothorax  will  be  found  under  the  head- 
ings dealing  with  these  conditions. 

Dilatation  of  the  bronchi  is  dependent  on  the  amount  of  fibrous  tissue 
which  develops  during  the  course  of  the  disease.  If  the  process  is  acute 
the  bronchi  present  no  change.  On  the  other  hand,  in  the  chronic  types 
of  the  disease  with  the  formation  of  much  fibrous  tissue  dilatation  of  the 
bronchi  is  not  uncommon. 


Fig.  237. — Thickened  pleura  at  apex  in  tuberculosis. 

Deformity  of  ;  he  chest  and  displacement  of  the  heart  depend  largely 
on  the  chronicity  of  the  disease.  If  chronic  and  there  is  much  fibroid 
tissue  present  the  affected  lung  shrinks  and  as  a  result  the  chest  wall 
becomes  retracted  and  the  heart  is  drawn  toward  the  diseased  side. 

Changes  in  Other  Organs. — In  addition  to  the  characteristic  changes 
which  are  seen  in  the  respiratory  organs,  tuberculosis  has  a  very  serious 
damaging  effect  on  other  organs  and  tissues  throughout  the  body.  The 
brief  account  which  follows  is  based  on  a  study  of  197  autopsied  cases 
by  C.  Y.  White.1     The  lesions  most  frequently  noted  are  the  presence  of 

1  Fifth  Report  of  Phipps  Institute,  1909. 


DISEASES    OF    THE    LUNGS  311 

tubercles,  usually  the  result  of  a  terminal  infection;  congestion;  catarrhal 
changes;  fatty  and  fibroid  degenerative  changes  and  ulceration.  In 
some  situations  all  of  these  changes  may  be  noted  while  in  others  one  or 
more  are  apt  to  be  present. 

The  larynx  is  frequently  the  seat  of  tuberculous  changes  in  dying 
cases.  Fetterolf l  in  a  special  study  of  100  cases  found  the  larynx  involved 
in  83  and  doubtfully  so  in  4.  In  the  trachea,  congestion  is  the  most  com- 
mon change  and  in  about  20  per  cent,  of  cases,  ulceration  is  present. 

Many  observers  hold  the  view  that  the  heart  in  tuberculosis  is  smaller 
than  normal  and  deduce  from  this  fact  that  the  size  of  the  heart  bears 
some  relation  to  susceptibility  to  the  disease.  Of  197  cases  the  weight  of 
the  heart,  for  both  males  and  females,  was  practically  that  of  the  average 
normal  heart.  Cardiac  changes  noted  at  the  autopsy  table  in  tuber- 
culosis are  about  the  same  as  those  encountered  under  other  conditions. 
In  about  half  the  cases  there  are  to  be  seen  varying  degrees  of  hypertrophy 
or  dilatation,  usually  the  latter,  of  one  or  more  of  the  chambers.  A  small 
proportion  show  thickening  of  the  valve  leaflets  and  in  a  still  smaller 
proportion,  the  valve  orifices  are  incompetent  or  stenosed.  Tuberculous 
infection  of  the  heart  muscle  is  rare.  (See  also  section  on  Tuberculosis 
of  the  Pericardium,  p.  606.) 

Next  to  the  lungs  the  g astro-intestinal  tract  and  its  associated  organs 
are  most  seriously  damaged.  This  leads  to  serious  defects  in  metabolism, 
with  consequent  lowered  nutrition.  Some  of  the  lesions  are  tuberculous, 
but  most  of  them  are  of  a  secondary  nature  and  because  of  the  fact  that 
they  are  so  general  and  extensive,  are  far  more  serious  to  the  functional 
activity  of  these  organs  than  the  lesions  which  are  distinctly  tuberculous 
in  character.  The  intestinal  tract  is  the  site  of  ulcerative  changes  in  from 
80  to  90  per  cent,  of  cases.  In  some  instances  a  large  portion  of  the  in- 
testinal mucous  membrane,  especially  the  lower  ileum,  may  be  the  site 
of  ulcerative  changes;  in  others  there  may  be  no  more  than  three  or  four 
ulcers.  The  stomach  is  the  site  of  an  ulcer  in  about  2  per  cent,  of  cases, 
which  is  about  the  usual  incidence  of  gastric  ulcer  under  all  conditions. 
Rarely  the  ulcer  is  tuberculous  in  character.  Pathological  changes  in 
the  esophagus  are  unusual.  Congestion  of  the  mucous  membrane  is 
occasionally  noted  and  in  a  few  instances  tubercle-like  nodules  are  seen 
(3  out  of  140  autopsies). 

The  secondary  changes  noted  in  the  gastro-intestinal  tract  are  sub- 
acute and  chronic  gastritis;  gastro-enteritis,  chronic  catarrhal  enteritis 
and  colitis.  Anatomical  changes  also  occur.  Gastroptosis  was  noted 
in  62  out  of  197  cases;  ptosis  of  the  large  gut  was  encountered  in  but  two 
cases. 

Tuberculous  changes  in  the  appendix  were  noted  in  10  out  of  197 
cases.  About  7  per  cent,  of  the  cases  showed  tuberculous  fistulse  in  the 
ischio-rectal  region.  Microscopical  examination  of  the  ischio-rectal 
region  also  showed  the  presence  of  a  high  percentage  of  tubercles  in  cases 
having  no  signs  of  fistula  or  abscess. 

The  parenchymatous  tissue  of  the  liver  and  pancreas  usually  shows 
widespread  lesions  varying  from  a  slight  cloudiness  to  complete  necrosis 
or  extensive  fatty  changes.  Accompanying  these  lesions  in  the  parenchy- 
matous tissue  there  is  generally  some  fibroid  change.  The  same  lesions 
are  noted  in  the  thyroid  and  suprarenal  glands,  both  of  which  are 
1  Trans.  Am.  Laryngological  Assoc,  1914. 


312      DISEASES   OF   THE  BRONCHI,    LUNGS,   PLEURA,   AND   DIAPHRAGM 

also  concerned  in  metabolism.  Amyloid  changes  in  the  liver  are  not 
uncommon. 

Although  the  liver  occasionally  shows  large  caseous,  tuberculous  foci, 
this  is  rare.  The  presence  of  minute  pinpoint  and  microscopic  tubercles 
is  very  common  and  probably  represents  a  terminal  infection.  The  pan- 
creas is  quite  resistant  to  the  tubercle  bacillus  but  even  this  organ  occa- 
sionally shows  microscopic  tubercles.  Tubercles  are  also  noted  in  the 
thyroid  gland  and  especially  in  the  suprarenals.  The  latter  may  also  be 
the  seat  of  large  caseous  tubercles  which  may  entirely  destroy  the  organ. 

The  spleen  is  usually  slightly  enlarged  and  often  congested.  Miliary 
tubercles  were  noted  in  60  and  amyloid  changes  in  51  out  of  197  cases. 

Chronic  inflammatory  changes  in  the  kidneys  are  extremely  common 
but  these  changes  do  not  differ  essentially  from  those  found  in  the  kidneys 
of  individuals  dying  of  other  chronic  diseases.  The  changes  are  brought 
about  by  the  extra  work  thrown  upon  the  kidneys  in  the  elimination  of 
the  toxic  products  generated  by  the  tubercle  bacilli  or  the  organisms 
of  mixed  infections  so  frequently  found.  In  addition  to  evidences  of 
nephritis  a  very  considerable  proportion  of  the  kidneys  also  show  the 
presence  of  small  miliary  tubercles. 

Other  portions  of  the  genito-urinary  tract,  in  both  the  male  and 
female,  seem  to  be  less  liable  to  infection  with  the  tubercle  bacillus  even 
in  the  terminal  stages.  Tuberculosis  of  the  testicle  rarely  occurs  in 
the  course  of  the  chronic  ulcerative  type  of  tuberculosis.  When  seen  it 
usually  dominates  the  clinical  picture,  the  pulmonary  disease  being  of 
secondary  importance. 

Involvement  of  the  meninges  is  not  common  in  the  chronic  ulcera- 
tive type  of  tuberculosis.  Meningeal  tuberculosis  is  most  often  seen 
in  acute  miliary  tuberculosis.  The  condition  is  relativeby  common  in 
children  and  it  is  very  frequently  the  terminal  event  in  cases  of  tuberculosis 
of  the  testicle. 

Symptoms. — Pulmonary  tuberculosis  has  no  distinctive  mode  of 
onset  nor  is  there  any  single  symptom  which  is  absolutely  pathognomonic 
of  the  condition.  In  some  instances  there  is  a  danger  signal  in  the  form 
of  a  single  symptom;  in  the  majority  of  cases,  however,  the  onset  is 
insidious  and  the  disease  may  have  caused  considerable  damage  before 
its  true  nature  is  recognized. 

A  properly  taken  history  should  include  information  as  to  the  occu- 
pation of  the  individual,  the  presence  or  absence  of  tuberculosis  in  the 
family,  an  account  of  past  illnesses,  and,  lastly,  but  of  the  utmost  im- 
portance, an  account  of  the  present  illness.  It  is  no  exaggeration  to 
state  that  from  the  history  alone  the  vast  majority  of  cases  of  early 
tuberculosis  can  be  recognized  definitely,  or  at  least  the  presence  of  the 
disease  can  be  strongly  suspected.  The  mathematical  chances  of  tubercu- 
losis being  present  are  overwhelming  in  the  case  of  any  individual  who 
has  an  hemoptysis,  an  attack  of  pleurisy,  a  fistula  in  ano,  or  transient 
attacks  of  slight  hoarseness,  and  this  holds  true  in  the  face  of  previous 
good  health  and  excellent  physical  condition.  These  single  symptoms 
may  be  followed  very  shortly  by  other  evidences  of  pulmonary  disease. 
Very  often,  however,  they  are  to  be  looked  upon  as  prodromal  symptoms, 
and  months  or  years  may  elapse  before  the  disease  manifests  itself  in 
an  active  form.  For  one  who  is  to  become  tuberculous  the  most  fortunate 
thing  is  the  occurrence  of  one  of  these  single  isolated  symptoms,  as  they 


DISEASES    OF    THE    LUNGS  313 

are  apt  to  appear  before  there  has  been  any  deterioration  in  health  and 
before  the  pulmonary  lesion  has  become  extensive.  The  significance 
of  these  manifestations  is  being  constantly  overlooked,  partly  because 
of  the  absence  of  other  corroborative  symptoms,  but  largely  because  of 
a  paucity  or  even  entire  absence  of  physical  signs. 

The  onset  of  pulmonary  tuberculosis  may  be  as  follows : 
1.  Hemoptysis  and  Blood-streaked  Sputum. — The  one  disease,  above 
all  others,  in  which  hemoptysis  most  frequently  occurs  is  pulmonary 
tuberculosis.  This  fact  has  been  emphasized  and  reemphasized  in  season 
and  out  of  season  and  yet  the  true  significance  of  this  sjmiptom  is  being 
overlooked  constantly.  Blood  spitting  is  apt  to  occur  in  the  great 
majority  of  cases  of  pulmonary  tuberculosis  at  some  time  during  the 
course  of  the  disease.  Among  5856  cases  seen  at  the  Phipps  Institute 
the  occurrence  of  an  hemoptysis  was  acknowledged  by  2790  (47.6  per 
cent.)  at  the  time  of  their  first  visit.  The  difficulty,  however,  lies  not 
with  the  self-evident  case  of  phthisis  but  with  those  instances  in  which 
the  blood  spitting  occurs  as  the  initial  symptom  and  before  there  has 
been  any  deterioration  of  health  or  the  development  of  marked  physical 
signs.  It  is  extraordinary  how  frequently  the  source  of  the  blood  is 
ascribed  to  a  bleeding  point  in  the  upper  air  passages  in  spite  of  the 
fact  that  there  is  ample  proof  that  hemorrhage  from  this  region  is  ex- 
cessively rare.  Although  the  apparent  health  of  the  patient  and  the 
absence  or  paucity  of  physical  signs  must  be  looked  upon  as  strong  factors 
in  influencing  physicians  against  a  diagnosis  of  tuberculosis,  the  most 
important  reason,  in  my  opinion,  is  moral  cowardice.  Many  will 
admit  of  a  knowledge  of  the  significance  of  a  hemoptysis  of  obscure 
origin  but  in  particular  cases  are  unable  to  bring  themselves  to  make  a 
diagnosis  without  other  corroborative  symptoms  and  signs.  In  this 
connection  Cabot's  admonition  is  worth  repeating:  "I  do  not  deny 
that  the  causes  of  hemoptysis  are  numerous,  but  I  assert  that  the  causes 
of  genuinely  obscure  hemoptysis  in  temperate  climates  may  be  reduced  to 
one — pulmonary  tuberculosis."  The  objection  may  be  raised  that 
among  the  conditions  which  simulate  tuberculosis  most  closely  blood 
spitting  is  a  very  common  symptom.  So  it  is — and  among  such  condi- 
tions may  be  mentioned  the  various  mycotic  infections,  bronchiectasis, 
fibrosis  of  the  lungs,  malignant  disease  and  distomatosis.  The  last- 
named  has  a  fairly  distinct  geographical  distribution  and  is  to  be  en- 
countered in  this  part  of  the  world  in  imported  cases  only.  Of  the 
other  conditions  closer  study  will  show  in  them  certain  differences,  par- 
ticularly in  regard  to  the  physical  signs,  which  will  often  serve  to  dis- 
tinguish them  from  tuberculosis.  The  real  test,  however,  lies  in  the 
examination  of  the  sputum.  Cases  presenting  the  symptoms  and  physical 
signs  of  tuberculosis  without  the  presence  of  tubercle  bacilli  in  the  sputum 
should  arouse  at  once  the  suspicion  of  some  other  origin  for  the  hemor- 
rhage. The  main  point  is  that  a  tentative  or  even  a  positive  diagnosis 
does  no  harm  in  case  the  source  of  the  hemorrhage  is  not  a  tuberculous 
infection.  On  the  other  hand,  a  negative  diagnosis  va&y  lull  the  patient 
into  a  false  security.  There  is  little  to  be  said  in  favor  of  the  attitude 
of  mind  which  favors  withholding  a  diagnosis  of  tuberculosis  in  such 
cases  because  such  an  opinion,  if  wrong,  places  a  stigma  on  the  patient. 
Failure  to  give  due  heed  to  it  more  often  ends  in  the  disease  progressing 
to  hopeless  incurability. 


314      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

Figs.  238  and  239  clearly  show  the  majority  of  the  causes  of  hemop- 
tysis. That  depicting  Strieker's  results  deals  with  a  body  of  men  pre- 
sumably healthy.     It  is  apparent  that  the  occurrence  of  blood  spitting 

TUBERCULOSIS  BHmHBHHHniHHBlHaH  848 

TRAUMA  B  11 

PNEUMONIA  ■  7 

HEART  DISEASE  ■  5 

BRONCHIECTASIS  I  4 

INFLUENZA  |  3 

SYPHILIS  I  3 

ABSCESS  AND  GAN- 
GRENE OF  THE 
LUNG 

HYDATID    CYST    OF) 
THE  LUNG  i  • 

IRRITATING    FUMES) 

INHALED  J 

Fig.  238. — Causes  of  hemoptysis  in  Prussian  soldiers.     (Cabot,  "Differential  Diagnosis," 

after  F.  Strieker.) 

BBaaHHHBMBHBVBHBSBHHl  1723 
MITRAL  DISEASE  ■HHHBBnHH  1177 

UNSPECIFIED  CAUSE  OUUI  183 

PULMONARY    THROM- 


BOSIS OR  EMBOLISM  J     ~m m ™  141 

PULMONARY  ABSCESS) 
OR  GANGRENE  J 

BRONCHIECTASIS  MB  08 

PNEUMONIA  B  52 

ANEURYSM  ■  22 

TRAUMA  i  17 

NEOPLASM  I  6 

Fig.  239. — Causes  of  hemoptysis,  Massachusetts  General  Hospital.     (Cabot,  "Differential 

Diagnosis.") 

in  such  individuals  points  overwhelmingly  to  tuberculosis,  the  percentage 
in  favor  of  this  diagnosis  being  95.8.  The  table  compiled  by  Cabot  from 
cases  admitted  to  the  Massachusetts  General  Hospital  shows  a  wider 
distribution  of  the  underlying  causes. 


DISEASES    OF    THE    LUNGS  315 

It  is  to  be  borne  in  mind,  however,  that  cases  of  obvious  tuberculosis 
are  not  admitted  to  this  hospital  and  that,  as  in  the  case  with  most 
hospitals,  patients  suffering  from  failing  compensation  form  a  very  high 
percentage  of  the  total  admissions.  Even  so,  tuberculosis  occupies  first 
place  with  a  percentage  of  50.  Furthermore  it  is  a  fair  inference  that 
the  majority  of  those  classed  as  "undetermined"  properly  belong  under 
the  tuberculous  group,  which  would  raise  the  percentage  considerably. 

2.  Pleurisy. — It  is  becoming  more  and  more  appreciated  that  an 
attack  of  pleurisy  with  or  without  effusion  should  arouse  one's  suspicion 
as  to  the  existence  of  a  pulmonary  tuberculosis.  At  one  time  the 
occurrence  of  primary  pleurisy  was  looked  upon  as  relatively  common. 
The  attack  may  be  without  an  apparent  exciting  cause  or  it  may  follow 
exposure  to  cold.  In  any  event  it  is  now  recognized  that  at  least  80 
per  cent,  of  such  pleurisies  are  tuberculous  in  origin.  A  pleural  effusion 
which  develops  insidiously  and  attains  a  large  size  before  recognition 
is  almost  certainly  tuberculous. 

The  records  of  the  large  insurance  companies  show  that  the  death  rate 
from  tuberculosis  of  the  lungs  among  persons  who  have  had  pleurisy 
within  five  years  prior  to  insurance  is  three  times  the  average  rate  for 
individuals  without  such  a  history. 

3.  I schio-rectal  Abscess  and  Fistula  in  Ano. — Proctologists  have  per- 
formed a  valuable  service  in  emphasizing  the  tuberculous  nature  of  the 
great  majority  of  abscesses  in  and  about  the  ischio-rectal  fossa.  The 
occurrence  of  a  pyogenic  infection  in  this  region  should  always  call  for 
a  careful  physical  examination  of  the  chest.  In  the  event  of  a  negative 
examination  the  patient  should  be  warned  as  to  the  possible  danger  and 
cautioned  as  to  his  mode  of  life.  Very  often  the  ischio-rectal  abscess 
will  precede  definite  pulmonary  symptoms  by  several  years. 

4.  Hoarseness. — This  may  be  the  very  first  intimation  of  pulmonary 
tuberculosis.  The  hoarseness  may  develop  without  definite  exposure 
to  cold  or  any  other  known  cause.  It  may  be  persistent  from  the  onset 
but  more  often  is  transient  in  character,  being  present  for  a  few  days  and 
then  disappearing  and  reappearing  again.  Very  often  the  hoarseness  is 
noticeable  for  a  part  of  the  day  only;  either  on  getting  up  in  the  morning 
or  late  in  the  day  or  after  much  talking.  A  laryngological  examination 
is  imperative  in  these  cases.  Nothing  is  more  fatal  than  to  assume  that 
the  laryngitis  is  due  to  a  "cold." 

The  occurrence  of  any  one  of  the  above-mentioned  symptoms  fur- 
nishes the  most  valuable  information  possible  as  to  the  presence  of  a 
pulmonary  tuberculosis.  Unless  it  can  be  shown  conclusively  that  they 
are  produced  by  something  else  there  should  be  no  hesitation  in  making 
a  diagnosis  of  tuberculosis.  Furthermore,  it  cannot  be  too  strongly 
emphasized  that  the  physical  appearance  of  the  patient  should  have  no 
influence  in  arriving  at  a  conclusion.  Only  too  frequently  plrysicians 
hesitate  to  commit  themselves  because  the  patient  presents  every 
appearance  of  health  and  the  pulmonary  signs  are  indefinite. 

Unfortunately  tuberculosis  is  far  more  often  characterized  by  an 
insidious  rather  than  an  abrupt  onset,  and  there  is  no  single,  striking 
symptom  upon  which  we  can  place  much  reliance.  Cases  with  an 
insidious  onset  may  manifest  themselves  in  a  variety  of  ways. 

1.  The  individual  catches  "cold"  which  instead  of  clearing^up  per- 
sists, or  just  as  it  seems  to  be  getting  better  a  fresh  "cold"  is  acquired 


316      DISEASES   OF  THE  BRONCHI,   LUNGS,   PLEURA,   AND   DIAPHRAGM 

Associated  with  the  cough,  which  may  be  dry  and  hacking  in  character, 
there  are  loss  of  weight,  anemia,  malaise  and  at  times  the  sputum  may 
be  blood-tinged.  In  some  instances  patients  themselves  neglect  these 
"colds,"  in  other  instances  although  they  seek  advice,  they  are  told 
they  are  suffering  from  bronchitis. 

It  cannot  be  sufficiently  emphasized  that  a  cough  which,  without 
complications,  persists  over  six  weeks  or  two  months  is  suspicious  at 
least;  if  it  is  associated  with  loss  of  weight,  slight  fever,  and  malaise, 
it  is  almost  certainly  tuberculous  in  origin. 

2.  In  another  group  the  dominant  symptoms  are  referred  to  the 
g astro-intestinal  tract.  Anorexia  is  common,  or  the  appetite  is  variable, 
being  sometimes  very  good  and  at  others,  poor.  Symptoms  of  indiges- 
tion are  annoying  and  usually  take  the  form  of  distention  after  eating, 
with  a  sense  of  discomfort  or  even  well-marked  pain  in  the  epigastric 
region.  Constipation  is  usually  present.  In  this  group  malaise,  pallor 
and  loss  of  weight  also  occur.  Cough  may  be  present  or  absent.  If 
present  it  is  usually  not  marked  and  its  significance  is  lost  sight  of,  because 
of  the  marked  gastric  symptoms.  Stomach  coughs  were  once  common, 
but  fortunately  little  is  heard  of  them  nowadays.  Indigestion  occurring 
in  an  individual  previously  free  from  any  such  disturbance  and  associated 
with  malaise,  loss  of  weight  and  cough,  should  lead  one  to  take  a  careful 
history  of  the  case  and  above  all  make  a  thorough  examination  of  the 
lungs. 

3.  A  third  group  is  comprised  of  those  cases  in  which  the  onset  is 
so  insidious  that  there  is  nothing  which  definitely  attracts  attention.  The 
condition  is  often  described  by  the  expression  "generally  run  down." 
A  careful  analysis  of  the  symptoms  in  this  group  usually  reveals  the 
following  facts:  Malaise  is  marked  and  the  individual  has  a  feeling  of 
being  constantly  tired,  even  when  awakening  after  a  good  night's  sleep; 
there  is  loss  of  weight  which  may  amount  to  10  or  15  pounds,  so  gradual, 
however,  that  the  patient  has  not  been  conscious  of  it;  there  is  usually 
some  pallor,  which  is  more  marked  in  the  morning;  cough  may  be  absent, 
or  if  present,  is  confined  to  the  morning  on  awakening;  and  lastly,  there 
may  be  occasional  attacks  of  indigestion.  The  most  significant  features 
are  the  malaise  and  gradual  loss  of  weight.  Patients  in  this  group 
frequently  escape  detection  in  the  incipient  stage  of  the  disease. 

In  women  disturbances  of  the  menstrual  junction  are  among  the 
early  symptoms.  Either  the  flow  becomes  scanty  and  irregular  in  its 
appearance  or  it  ceases  entirely.  Under  the  same  circumstances  leukor- 
rhea  may  appear  or  if  already  present  become  greatly  aggravated. 

4.  The  attack  may  begin  more  abruptly  and  resemble  in  every  respect 
typhoid  fever.  The  patient  feels  tired  and  dragged  out  and  there  is  slight 
fever  which  finally  assumes  the  continuous  type  seen  in  typhoid  patients. 
Inasmuch  as  bronchitis  and  some  cough  are  commonly  present  in  typhoid 
fever  patients  the  true  nature  of  these  symptoms  are  overlooked.  I 
recall  one  patient  who  was  treated  for  nearly  three  weeks  for  typhoid 
fever,  without  a  suspicion  as  to  the  true  nature  of  his  trouble,  until  he 
had  a  fair-sized  pulmonary  hemorrhage  following  a  cold  bath.  This 
patient  had  a  moderately  advanced  lesion  in  the  right  upper  lobe  and 
tubercle  bacilli  in  the  sputum. 

I  think  there  can  be  but  little  doubt  that  tuberculosis  not  infrequently 
undergoes  an  acute  exacerbation  which  closely  resembles  an  attack  of 


DISEASES    OF   THE    LUNGS  317 

typhoid  fever.  Very  often  the  acute  process  spontaneously  subsides  and 
the  patient  apparently  makes  a  perfect  recovery.  Out  of  5895  cases  of 
tuberculosis  seen  at  the  Phipps  Institute  1083  or  18.3  per  cent,  gave  a 
history  of  having  had  typhoid  fever.  It  is  quite  likely  that  not  a  few  of 
these  were  instances  of  an  acute  exacerbation  of  tuberculosis. 

5.  Occasionally  tuberculosis  first  manifests  itself  with  chills,  fever 
and  sweats  which  may  assume  a  periodicity  similar  to  that  seen  in  malaria. 
In  regions  where  both  diseases  coexist  mistakes  are  frequent. 

6.  What  is  known  as  Louis'  law  should  be  borne  in  mind,  namely, 
that  after  the  age  of  puberty  a  tuberculous  lesion  in  any  part  of  the  body 
is  almost  invariably  accompanied  by  pulmonary  tuberculosis.  There- 
fore, the  presence  of  a  tuberculous  testicle  or  of  tuberculous  lymph  nodes 
in  an  adult  should  suggest  a  careful  examination  of  the  lungs. 

7.  Finally,  the  following  precepts  of  Dieulafoy  should  be  kept  in 
mind :  Every  youth  or  adult,  who  wastes  much  or  rapidly,  with  or  without 
fever,  must  be  suspected  of  having  tuberculosis,  in  the  absence  of  diabetes 
or  Basedow's  disease. 

Every  girl  or  young  woman  who  has  neither  genuine  chlorosis, 
Bright's  disease  nor  syphilitic  anemia,  but  yet  has  the  appearance  of 
chloro-anemia,  must  be  suspected  of  having  tuberculosis. 

The  symptoms  detailed  above  in  the  various  modes  of  onset  also  form 
the  symptomatology  of  the  incipient  stage.  If  the  disease  is  arrested  at 
this  stage  the  symptoms  disappear.  If,  however,  the  disease  progresses 
the  symptoms  already  present  are  apt  to  become  more  marked ;  the  ema- 
ciation becomes  more  pronounced,  the  cough  and  expectoration  more 
troublesome,  and  in  addition  new  symptoms  are  constantly  developing. 
By  the  time  the  terminal  stage  is  reached  the  patient  will  suffer  at  one 
time  or  another  from  all  of  the  symptoms  peculiar  to  the  disease. 

The  symptoms  of  tuberculosis  are  of  two  kinds:  (1)  the  general  or 
constitutional  symptoms  due  to  the  toxic  effects  of  the  infection;  and 
(2)  the  local  subjective  symptoms  due  to  pathological  changes  in  the 
various  organs. 

Constitutional  Symptoms. — Fever.— This  is  the  most  important  symp- 
tom in  tuberculosis  and  a  study  of  its  manifestations  yields  much  infor- 
mation, as  from  this  one  symptom  it  is  possible  to  trace  with  reasonable 
certainty,  the  destructive  process  of  the  disease  as  it  progresses  from  its 
incipiency  to  the  terminal  stages.  On  the  other  hand,  the  subsidence  of 
the  fever  is  the  most  reliable  evidence  we  have  that  the  disease  is  tending 
toward  arrest  or  quiescence. 

The  early  febrile  manifestations  of  tuberculosis  usually  consist  of 
slight  elevations  of  temperature  amounting  to  from  1°  to  2.6°F.  The 
fever  may  be  present  every  day  or  only  every  second  or  third  day  (see 
Fig.  240) .  It  is  increased  by  exercise  and  as  a  rule  quickly  subsides  after 
several  weeks'  rest  in  bed.  At  times  slight  fever  persists  in  an  early  case 
even  after  prolonged  rest  (see  Fig.  241).  This  is  usually  an  indication  of 
poor  resistance  or  the  presence  of  more  extensive  disease  than  the  physical 
signs  indicate. 

Very  often  the  febrile  stage  is  succeeded  by  a  period  of  subnormal 
temperature  during  which  time  the  patient  continues  to  improve  (see 
Fig.  242).  Gradually  the  temperature  curve  shows  less  marked  remis- 
sions and  becomes  normal.  Unless  a  relapse  occurs  or  there  is  some 
intercurrent  disturbance  the  temperature  then  remains  normar.     Sub- 


318      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND  DIAPHRAGM 

normal  temperatures  are  also  present  in  cases  with  advanced  disease 
which  is  temporarily  quiescent.  In  such  instances  the  vitality  is  usually 
poor. 


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Fig.   240. — Temperature  in  an  early  case  with  lesion  at  right  apex. 


A.M. 

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Fig.  241. — Persistent  slight  fever  in  an  early  case  after  prolonged  rest  in  bed. 


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Fig.  242. — Subnormal  temperature  often  noted  after  subsidence  of  fever  in  early  cases 


A  pulmonary  hemorrhage  may  be  followed  by  fever.  This  may  be 
due  to  an  acute  respiratory  infection  which  has  been  the  exciting  cause  of 
the  hemorrhage  or  it  may  result  from  small  areas  of  broncho-pneumonia 
due  to  insufflation  of  blood. 


DISEASES    OF   THE    LUNGS 


319 


In  persons  who  have  become  afebrile,  an  abrupt  rise  in  the  tem- 
perature may  occur  and  last  for  a  day  or  so.  This  may  be  due  to  an  acute 
cold  (see  Fig.  243),  some  gastric  disturbance,  constipation,  slight  pleurisy, 
overexertion,  etc.  In  women  during  the  active  stage  of  the  disease  the 
temperature  may  abruptly  rise  some  days  prior  to,  or  with  the  onset  of, 
the  menstrual  period  (see  Fig.  244)  and  may  remain  elevated  until  the  flow 
ceases.     In  patients  who  have  been  afebrile,  and  in  whom  these  temporary 


A.M.    ■ 

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Fig.  24.3. — Afebrile  case.     Rise  in  temperature  due  to  acute  cold. 


102° 


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fe 


I: 


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Fig.  244. — Rise  in  temperature  due  to  menstruation. 

manifestations  of  fever  occur,  it  is  usually  an  indication  that  the  disease 
has^not  become  arrested  but  is  simply  quiescent.  When  they  can  pass 
through  such  episodes  without  a  febrile  reaction,  it  may  be  taken  as  one 
of  the'fpieces  of  evidence  that  the  disease  is  apparently  arrested. 

When  the  disease  is  not  arrested  but  continues  to  spread  the  tem- 
perature is  moderately  high  and  may  be  intermittent,  remittent  or 
continuous  (see  Fig.  245).  The  temperature  may  then  subside  and 
become  normal  or  show  but  slight  elevations  or  it  may  pass  into  the.  hectic 
type  which  is  characterized  by  marked  remissions  and  intermissions 


320      DISEASES   OF   THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 


M|E  Ml E  Ml E  M|E  Ml E  Ml E  m|E  MJEMEMEME  Ml E  M  E  M|E|m|E  M  E  M ' E I M ' E I M ' E ' M I E I M I E 


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Fig.  246. — Intermittent  and  remittent  type  of  temperature  seen  in  advanced  cases. 


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Fig.  247. — Rapidly  advancing  process  of  bronchopneumonia  type.     Also  shows  inverted 

temperature. 


DISEASES    OF    THE    LUNGS 


321 


(Fig.  246).  In  this  type  of  temperature,  which  is  always  present  in 
advanced  cases  which  are  progressing  toward  a  fatal  termination,  the 
difference  between  the  morning  and  evening  temperature  may  amount 
to  from  5°  to  8°F. 

When  new  areas  of  lung  tissue  are  being  invaded  the  temperature 
is  continuous  in  type,  sometimes  with  slight  remissions  and  in  other 
instances  there  are  marked  intermissions  (Figs.  247  and  248).     Such  tern- 


A.M. 

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Fig.  248. — Rapidly  advancing  type  of  disease      Also  shows  inverted  temperature. 


1 

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Fig.  249. 


-Temperature  curve  resembling  that  of  lobar  pneumonia.     In  this  case  the 
temperature  fell  to  normal  in  three  weeks. 


perature  curves  always  indicate  marked  activity  of  the  disease.  Tem- 
peratures of  this  type  may  be  present  when  the  case  is  first  seen  or 
develop  after  a  period  of  slight  fever;  as  a  rule  they  change  into  the 
hectic  type  but  the  fever  may  gradually  subside  and  the  temperature 
become  normal.  Another  interesting  feature  to  be  looked  for  in  charts 
of  this  type  is  inversion  of  the  temperature,  that  is  the  morning  tempera- 
ture is  higher  than  that  in  the  evening.     An  inverted  temperature  is  com- 


322      DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND   DIAPHRAGM 

monly  associated  with  miliary  tuberculosis  but  it  often  may  be  noted 
in  pulmonary  cases  in  which  the  disease  is  spreading  rapidly.  It  is  not 
constant  and  is  usually  observed  but  a  few  days  as  shown  in  both 
Figs.  247  and  248. 

Another  type  of  temperature  is  that  seen  in  cases  with  an  acute  onset 
and  high  fever.  The  fever  may  subside  by  lysis  in  two  or  three  weeks 
(see  Fig.  249)  or  it  may  become  hectic  in  type.  Such  cases  are  not  in- 
frequently mistaken  for  lobar  pneumonia  because  of  the  sudden  onset, 
high  fever,  blood  in  the  sputum  and  signs  of  consolidation  over  an  upper 
lobe. 

A  continuous  type  of  temperature  which  is  broken  at  intervals  by 
marked  intermissions  (Fig.  248)  sometimes  leads  to  a  diagnosis  of  malaria, 
especially  when  the  sudden  rises  in  the  temperature  are  accompanied  by 
chilly  sensations. 


A.M. 

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Fig.  250. — Type  of  temperature  seen  in  terminal  stage  of  advanced  cases. 


In  the  terminal  stage  of  the  disease  the  temperature  is  characterized 
by  marked  irregularities,  such  as  shown  in  Fig.  250. 

The  diagnostic  and  prognostic  value  of  temperature  observations 
cannot  be  overestimated.  The  clinical  thermometer  should  always  be 
used.  In  the  very  early  cases  when  the  symptoms  and  physical  signs 
are  inconclusive,  the  use  of  the  thermometer  three  or  four  times  a  day 
for  a  week,  will  often  determine  the  diagnosis.  Furthermore,  the  absence 
of  fever  in  cases  with  other  unequivocal  evidences  of  the  disease,  or  the 
rapid  subsidence  of  fever  are  the  best  evidences  we  possess  of  an  inactive 
type  of  disease.  The  temperature  should  always  be  taken  in  the  morning 
and  again  in  the  afternoon,  preferably  at  4  p.m.  Additional  observations 
may  be  made  at  noon  and  8  p.m.  if  thought  necessary. 

Although  the  use  of  the  clinical  thermometer  is  a  simple  procedure 
certain  precautions  should  be  observed.     Not  infrequently  I  have  been 


DISEASES    OF    THE    LUNGS  323 

told  that  a  patient  had  no  fever  when  subsequent  observations  in  a  sana- 
torium showed  that  there  was  a  slight  rise  in  the  temperature  every 
afternoon.  In  order  to  detect  slight  rises  in  the  temperature  (99°  to 
99.3°F.)  the  thermometer  should  be  left  in  the  mouth  not  less  than  10 
minutes.  For  temperatures  over  100°F.  any  thermometer  will  register 
the  amount  of  fever  within  a  minute,  but  for  slight  elevations  even  the 
half  minute  and  minute  thermometers  will  often  fail.  Several  years 
ago  I  carried  out  a  series  of  observations  which  showed  that  a  3-minute 
thermometer,  if  kept  in  the  mouth  for  at  least  10  minutes,  was  for  prac- 
tical purposes,  as  accurate  as  the  quickly  registering  thermometers 
placed  in  the  rectum.  Mouth  temperatures  should  not  be  taken  within 
half  an  hour  if  the  patient  has  taken  anything  very  hot  or  very  cold  to 
eat  or  drink. 

Many  observers  recommend  the  rectal  use  of  the  thermometer  as  the 
only  reliable  method.  If  the  precautions  I  have  given  are  observed  this 
will  not  be  necessary.  Besides  it  is  less  convenient  and  often  patients 
object  to  it. 

.  Loss  of  Weight.- — A  gradual  and  progressive  loss  of  weight  is  charac- 
teristic of  the  disease.  The  amount  lost  varies  greatly  in  different 
individuals  and  is  governed  to  a  large  extent  by  the  severity  of  the  infec- 
tion. In  the  acute  types  of  the  disease  the  loss  is  rapid  and  may  eventu- 
ally amount  to  a  third  or  more  of  the  normal  body  weight.  In  the 
chronic  forms  of  the  disease  the  loss  of  weight  is  rarely  extreme  and  in 
addition  it  is  apt  to  be  quickly  regained  if  the  patient  is  put  under  the 
proper  treatment.  A  progressive  loss  of  weight  which  continues  in  spite 
of  proper  treatment  is  always  of  serious  import.  On  the  other  hand,  a 
steady  gain  in  weight  is  one  of  the  most  favorable  prognostic  signs. 

Not  only  does  the  patient  show  emaciation  but  the  muscular  system 
becomes  more  and  more  atrophied  as  the  disease  progresses.  In  addi-' 
tion  the  muscles  become  unduly  irritable. 

Malaise. — In  many  cases  with  an  insidious  onset  a  sense  of  weariness 
with  or  without  exertion  of  any  kind  may  be  the  first  manifestation  of 
the  disease.  Very  often  it  is  the  only  symptom  the  patient  complains 
of  for  months.  It  is  the  one  symptom  that  has  walked  more  patients 
into  their  graves  than  any  other  because  of  the  fact  that  exercise  is 
almost  invariably  prescribed.  This  is  commonly  done  without  attempt- 
ing to  find  out  whether  there  are  any  associated  symptoms.  The  exer- 
cise is  prescribed  on  the  ground  that  inasmuch  as  it  makes  a  healthy 
man  feel  better  it  ought  to  make  the  individual  who  is  suffering  from 
languor  feel  twice  as  well.  Unfortunately  this  procedure  aggravates 
the  difficulty  instead  of  relieving  it.  As  the  disease  progresses  the  sense 
of  languor  and  tiredness  increases.  In  the  terminal  stages  of  the  disease 
it  is  due  to  the  extreme  emaciation  and  inability  to  absorb  the  proper 
amount  of  nourishment. 

Closely  allied  to  this  condition  of  general  malaise  is  neurasthenia.  It 
is  becoming  more  and  more  recognized  that  neurasthenia  is  rarely  a  pure 
functional  disturbance.  In  some  cases  of  tuberculosis,  neurasthenia  is 
a  very  marked  feature  of  the  disease  and  the  nervous  phenomena  may 
dominate  the  picture.  On  the  other  hand,  there  are  many  cases  of 
neurasthenia  which  are  considered  as  instances  of  a  functional  disturb- 
ance of  the  nervous  system  but  which  in  reality  are  due  to  a  latent  tuber- 
culous infection  which  escapes  notice.     I  recall  one  case  in  which  neuras- 


324       DISEASES   OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND   DIAPHRAGM 

thenia,  associated  with  profound  asthenia,  had  existed  for  four  years. 
Although  the  neurologist  in  charge  suspected  a  tuberculous  infection  it 
could  never  be  located.  Finally  the  occurrence  of  an  hemoptysis  pointed 
to  pulmonary  trouble  which  a  careful  physical  examination  snowed  to  be 
present  in  the  apex  of  the  right  lung.  The  patient  was  then  treated  as  a 
case  of  tuberculosis  and  made  a  complete  recovery. 

Night  sweats  may  occur  at  any  time  during  the  course  of  the  disease 
but  are  not  usually  encountered  in  the  incipient  stage.  They  occur  very 
commonly  in  the  second  stage  but  as  a  rule  are  not  severe.  Sweating 
varies  greatly  in  different  individuals.  In  some  cases  it  is  the  most  dis- 
tressing and  harassing  manifestation  of  the  disease,  as  it  is  not  only  ex- 
hausting but  in  addition  causes  great  discomfort.  As  a  rule  night  sweats, 
which  do  not  disappear  after  the  patient  has  been  put  under  treatment, 
occur  in  the  acute  types  of  the  disease  and  in  the  terminal  stages  of  the 
chronic  form  when  fever  is  present.  Sweating  rarely  occurs  in  an  afeb- 
rile patient.  Night  sweats,  as  the  name  implies,  occur  at  night,  usually 
in  the  early  morning  hours. 

Axillary  sweating  is  very  common  in  tuberculous  subjects  even  in 
the  incipient  stage  of  the  disease.  A  tendency  to  sweat  after  the  least 
exertion  is  also  of  frequent  occurrence  during  the  early  stages  of  the 
disease. 

Chills. — Sometimes  chills  occur  as  an  early  manifestation  of  the 
disease.  As  a  rule  chills  associated  with  fever  and  sweats,  occur  in  very 
acute  types  of  the  disease,  such  as  pneumonic  phthisis  and  acute  miliary 
tuberculosis.  In  the  terminal  stage  of  chronic  ulcerative  tuberculosis, 
while  chilly  sensations  are  not  infrequent,  distinct  chills  are  unusual. 

Anemia. — A  slight  degree  of  anemia  in  the  incipient  stage  of  tubercu- 
losis is  not  uncommon,  although,  as  a  rule,  it  is  more  apparent  than  real. 
Morning  pallor  is  often  very  noticeable;  this  is  apt  to  be  masked  in  the 
afternoon  by  flushing  of  the  cheeks  as  the  result  of  slight  fever. 

In  the  second  and  third  stages  of  the  disease  anemia  may  or  may  not 
be  present.  Sometimes  it  is  quite  marked.  In  other  instances  and  espe- 
cially in  individuals  who  have  been  under  appropriate  treatment,  there 
is  no  evidence  of  anemia;  on  the  contrary,  the  patients  often  present  a 
healthy,  ruddy  color. 

The  blood  picture  in  tuberculosis  has  a  slight  resemblance  to  that 
seen  in  chlorosis  in  that  the  hemoglobin  is  most  affected,  although  the 
reduction  of  the  hemoglobin  content  in  tuberculosis  is  never  as  marked  as 
in  chlorosis.  The  leukocytes  in  tuberculosis  are  not  increased  in  the 
first  and  second  stages;  in  the  third  stage  a  moderate  leukocytosis  is 
common,  probably  as  the  result  of  mixed  infection. 

G 'astro-intestinal  Sympto?ns.- — As  already  mentioned  these  symptoms 
may  overshadow  the  pulmonary  symptoms  at  the  onset  of  the  disease. 
Anorexia  is  not  uncommon  in  the  beginning  and  may  persist  until  the 
end.  In  some  patients  gastric  disturbances  persist  or  recur  very  fre- 
quently throughout  the  course  of  the  disease  and  seriously  interfere  with 
recovery.  The  majority  of  people  suffering  from  tuberculosis  give  both 
subjective  and  objective  evidence  of  the  injury  which  befalls  the  ali- 
mentary canal  and  the  organs  which  have  to  do  with  nutrition.  A  coated 
or  dry  tongue,  loss  of  appetite,  nausea  and  vomiting,  constipation,  and 
diarrhea  are  the  common  symptoms  which  are  encountered.  One  or  the 
other  of  them  exists  in  almost  every  case.     As  a  general  rule  it  can  be 


DISEASES    OF    THE    LUNGS  325 

said  that  the  chances  of  recover}'  are  very  poor  if  the  patient  either  can- 
not eat  because  of  marked  anorexia  or  because  the  least  thing  upsets  the 
stomach.  In  spite  of  extensive  disease  of  the  lungs  and  marked  symp- 
toms some  patients  continue  to  have  a  good  appetite  and  digest  their 
food  without  discomfort.  In  those  who  suffer  from  a  sense  of  fulness, 
often  with  considerable  epigastric  pain  after  eating,  the  trouble  is  rarely 
due  to  pathological  changes  in  the  stomach  but  to  alterations  in  the  char- 
acter of  the  gastric  juice.  The  gastric  juice  may  be  inefficient  because 
it  is  too  small  in  amount  or  too  poor  in  quality.  At  times  nausea  and 
vomiting  may  occur  but  more  often  the  patient  simpfy  feels  nauseated 
either  at  the  sight  of  food  or  after  eating.  Vomiting  more  often  results 
from  a  reflex  action  as  the  result  of  a  paroxysm  of  coughing.  In  the 
effort  to  build  the  patient  up  forced  feeding  is  sometimes  injudiciously 
employed  with  the  result  that  the  overfeeding  produces  a  typical  bilious 
attack. 

Diarrhea  is  sometimes  a  very  troublesome  symptom.  It  may  be 
due  simply  to  a  catarrhal  inflammation  of  the  intestinal  mucous  membrane 
or  as  the  result  of  intestinal  ulceration.  It  may  be  stated,  however,  that 
diarrhea  even  when  most  severe,  cannot  be  taken  as  an  indication  of 
tuberculous  ulceration  of  the  intestines. 

Cardio-vascular  Symptoms. — Acceleration  of  the  pulse  is  a  very  fre- 
quent manifestation  in  tuberculosis.  It  may  occur  as  an  early  symptom 
and  without  fever.  Under  these  circumstances,  it  is  of  value  as  an  early 
diagnostic  sign.  As  the  disease  progresses  the  tendency  of  the  pulse 
rate  to  increase  becomes  more  marked.  In  some  instances  the  patient 
is  not  conscious  of  the  rapidly  beating  heart  but  at  times  an  annoying 
palpitation  occurs  with  the  tachycardia.  During  the  last  stage  of  the 
disease  the  pulse  rate  is  usually  very  high  rising  to  120  or  more. 

The  blood-pressure  in  tuberculous  subjects  is  usually  low.  If  the 
disease  undergoes  arrest  and  health  is  restored,  the  blood-pressure  returns 
to  normal.  Cardiac  weakness  is  not  uncommonly  present  and  occa- 
sionally is  the  cause  of  death. 

Edema  of  the  extremities,  especially  the  legs,  is  not  infrequently  seen 
in  the  terminal  stage  of  tuberculosis.  It  is  always  an  indication  that  the 
end  is  near  at  hand.  Edema  may  be  due  to  cardiac  weakness,  a  com- 
plicating nephritis  or  both. 

A  violet  or  bluish  discoloration  of  the  nails  is  frequently  noted. 
When  it  occurs  in  the  early  stages  of  the  disease  it  is  usually  an  indica- 
tion that  the  infection  is  a  serious  one.  It  is  almost  invariably  present 
in  the  terminal  stage.  While  the  condition  resembles  cyanosis  due  to 
cardiac  weakness  it  occurs  independently  of  the  heart  and  is  apparently 
due  to  toxic  absorption.  True  cyanosis  of  the  fingers  and  lips  is 
occasionally  noted. 

Skin. — In  the  early  stages  of  the  disease  the  skin  rarely  shows  any 
abnormality.  In  the  advanced  stages,  however,  it  is  nearly  always 
unduly  dry  or  moist  and  clammy.  Often  the  skin  has  a  scaly  appearance 
and  fine  bran-like  flakes  can  be  scraped  off.  In  those  who  are  uncleanly 
in  their  habits  pityriasis  versicolor,  an  eruption  which  consists  of  yellow- 
ish or  orange-colored  patches,  is  commonly  seen  on  the  thorax  and  upper 
abdomen. 

Jaundice  and  purpura  are  occasionally  noted  in  tuberculosis;  usually 
in  the  terminal  stage.     In  an  analysis  of  the  ward  patients  in  the  Phipps 


326      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

Institute,  Cruiee  found  7  instances  of  jaundice  among  1748  cases  and  8 
of  purpura  among  1626  cases. 

A  hectic  flush  is  common  in  the  afternoon  even  in  patients  who  have 
a  very  slight  rise  in  the  temperature.  The  flush  is  usually  confined  to 
the  side  affected  or  if  both  lungs  are  involved  will  be  more  marked  on  the 
side  having  the  most  marked  disease.    . 

In  advanced  cases  the  hair  becomes  thin  and  presents  a  dry,  lusterless 
appearance. 

Urine. — In  the  early  cases  evidences  of  kidney  irritation  occur  with  no 
greater  frequency  than  is  encountered  in  the  general  run  of  individuals. 
As  the  tuberculous  process  advances,  however,  the  urinary  findings  show 
an  increasing  number  of  abnormalities.  Walsh  found  albumen  present 
in  47  per  cent,  of  advanced  cases  and  casts  are  nearly  as  frequently  present. 
In  a  small  percentage  of  cases  sugar  is  present.  It  was  noted  in  2  per 
cent,  of  656  cases  studied  at  the  Phipps  Institute.  In  some  instances 
it  is  due  to  a  true  diabetes;  in  others  it  is  to  be  looked  upon  as  a  mild 
glycosuria. 

Ehrlich's  diazo  reaction  was  considered  at  one  time  to  be  of  both 
diagnostic  and  prognostic  value.  As  it  is  often  found  in  conditions  other 
than  tuberculosis,  it  has  no  significance  as  a  diagnostic  sign;  and  the 
same  may  be  said  of  its  prognostic  value. 

Phosphaturia  is  often  present  when  the  patient  is  steadily  losing 
weight.     It  is  looked  upon  as  an  evidence  of  cell  destruction. 

Nervous  System. — The  mental  attitude  varies  greatly.  This,  however, 
has  little  to  do  with  the  disease  itself;  for  while  it  is  true  that  most  people 
are  depressed  at  the  onset,  they  rapidly  revert  to  their  normal  state  of 
mind.  This  maj^  be  optimistic,  pessimistic  or  indifferent  as  the  case 
may  be.  It  is  a  common  belief  that  the  spes  phthisica  is  of  frequent 
occurrence  in  tuberculous  subjects.  It  is  extraordinary  how  some  patients 
will  cheerfully  make  plans  for  the  future  even  when  they  are  a  few  days 
from  death.  Although  the  frequency  of  this  exaggerated  form  of  hope- 
fulness has  been  greatly  overestimated,  it  is  undeniably  true  that  cheer- 
fulness and  optimism  as  to  the  outcome,  is  more  often  present  than 
depression  and  pessimism. 

Tuberculosis  among  the  insane  is  very  common  but  no  more  so  than 
a  similar  group  of  individuals  living  under  like  circumstances.  On  the 
other  hand  the  development  of  a  psychosis  in  a  tuberculous  subject  is 
relatively  infrequent.  McCarthy  recognizes  a  small  group  of  psychoses 
due  to  tuberculosis  and  a  second  group  which  includes  the  usual  type 
of  insanity  determined  by  a  lowering  of  nutrition.  The  first  group  pre- 
sents a  symptom  complex  closely  resembling  paresis.  In  the  second  group 
the  psychosis  may  take  the  form  of  melancholia,  mania,  dementia  prsecox, 
hysterical  insanity  and  delusional  insanity.  Suicidal  tendencies  are  not 
uncommon  especially  in  those  who  become  depressed  and  melancholy. 

Hypercesihesia. — Points  of  tenderness  may  occur  in  various  parts 
of  the  body  and  in  some  instances  there  is  a  definite  neuritis. 

Herpes  zoster  is  occasionally  noted  in  tuberculosis  but  it  is  doubtful 
whether  the  condition  can  be  ascribed  to  the  tuberculous  infection.  Head- 
ache is  not  infrequent.  It  is  commonly  due  to  eye  strain  and  is  usually 
encountered  in  those  confined  to  bed  and  who  read  a  great  deal.  Per- 
sistent headache  should  always  arouse  suspicion  as  to  the  presence  of  a 
meningitis. 


DISEASES    OF    THE    LUNGS  327 

Insomnia  of  a  mild  grade  is  not  uncommon;  it  is  rarely  severe  enough 
to  demand  treatment.  The  sleep  is  often  broken,  however,  by  night 
sweats  or  attacks  of  coughing. 

Arthritis,  generally  affecting  the  ankles,  is  in  my  experience  relatively 
common  in  advanced  cases.  The  ankles  become  slightly  swollen,  red- 
dened and  very  painful.  In  some  instances  the  pain  is  intense  and  even 
the  weight  of  a  sheet  is  unbearable.  A  number  of  French  observers 
look  upon  this  type  of  arthritis  as  being  tuberculous  in  origin. 

Menstrual  Function. — In  women  the  menstrual  function  is  affected 
sooner  or  later,  in  the  majority  of  cases.  Sometimes  suppression  of  the 
menses  is  one  of  the  earliest  manifestations  of  the  disease.  As  a  rule, 
the  menstrual  flow  first  becomes  irregular  and  scanty  and  finally  ceases. 
If  the  patient  is  restored  to  health  the  menstrual  function  gradually 
becomes  normal.  Leukorrhea  is  also  apt  to  develop  or  if  present  it 
becomes  much  worse. 

Local  Subjective  Symptoms. — Cough. — In  the  majority  of  cases  cough 
is  among  the  very  earliest  manifestations  of  the  disease  and  is  usually 
the  first  symptom  that  the  patient  notices.  At  first  it  may  be  confined 
to  the  morning  on  awakening  or  it  may  be  absent  at  that  time  and  occur 
intermittently  during  the  day.  In  still  other  instances  it  is  most  marked 
on  going  to  bed.  Not  infrequently  what  is  at  first  believed  to  be  an 
acute  cold  continues  indefinitely.  It  is  a  safe  rule  to  view  any  cough 
which  persists  for  six  weeks  or  two  months  as  being  tuberculous  in  origin 
unless  the  contrary  can  be  proved  definitely.  As  the  disease  progresses 
the  cough  becomes  more  and  more  severe  and  tends  to  become  paroxysmal 
in  character. 

Occasionally  the  patient  has  a  number  of  symptoms  indicating  the 
existence  of  an  incipient  tuberculosis  and  no  cough  whatever.  The  cough 
is  due  to  the  irritation  of  the  bronchial  mucous  membranes  by  the  pul- 
monary secretions  and  is  almost  invariably  relieved  by  the  expulsion  of 
the  sputum.  Any  cough  which  is  unproductive  is  largely  unnecessary 
and  can  be  controlled  voluntarily  to  a  great  extent  by  the  patient. 

Expectoration. — As  a  rule  the  cough  and  expectoration  are  closely 
associated  and  the  one  is  almost  invariably  accompanied  by  the  other. 
There  may  be  considerable  expectoration,  however,  with  little  or  no 
cough,  the  sputum  being  brought  up  by  what  is  known  as  hawking  or 
clearing  the  throat.  In  the  early  stages  of  the  affection  the  sputum 
is  usually  slight  in  amount  but  as  the  disease  progresses  it  becomes  more 
and  more  profuse,  especially  after  the  formation  of  a  cavity. 

As  to  the  sputum  in  tuberculosis  it  can  be  said  that  it  has  no  dis- 
tinctive characteristic,  except  possibly  in  the  stage  of  excavation,  when 
the  so-called  nummular  sputum  occurs.  The  latter  is  brought  up  in 
the  form  of  irregularly  shaped  grayish  or  greenish-gray  balls  which 
sink  in  water.  Sputum  with  similar  characteristics  may  occur  also  in 
bronchiectasis. 

Aside  from  this  form  of  sputum  the  secretion  may  consist  of  glairy 
transparent  material  with  black  specks  scattered  through  it;  it  may  be 
slightly  or  markedly  yellowish  in  color  and  later  it  may  assume  a  greenish 
tinge.  From  time  to  time  blood  may  be  noted  in  the  sputum.  The 
blood  may  occur  in  the  form  of  a  few  minute  specks;  it  may  be  in  the  form 
of  streaks  or  the  blood  may  be  intimately  mixed  with  the  sputum  giving 
it  a  pinkish  or  reddish  color,  depending  on  the  amount  of  blood  present. 


328       DISEASES    OF   THE   BRONCHI,    LUNGS;    PLEURA,    AND    DIAPHRAGM 

Hemoptysis.- — The  significance  of  hemoptysis  has  been  alluded  to  in 
considering  the  modes  of  onset.  Hemoptysis  occurs  in  about  one-half 
of  all  cases  of  pulmonary  tuberculosis,  although  some  observers  have 
placed  the  incidence  as  low  as  30  per  cent,  and  others  as  high  as  80  per 
cent.  Of  5856  cases  observed  at  the  Phipps  Institute  47.6  per  cent, 
had  had  an  hemoptysis  at  some  time  during  the  course  of  the  disease. 

Males  are  somewhat  more  liable  to  hemoptysis  than  females,  probably 
because  of  their  greater  physical  activity.  The  accident  occurs  most 
frequently  in  adults  who  are  suffering  from  the  chronic  ulcerative  type  of 
disease.  Hemoptysis  is  an  unusual  occurrence  in  children  nor  is  it  often 
noted  in  the  acute  types  of  the  disease  in  adults. 

The  amount  of  the  hemorrhage  varies  greatly.  It  may  consist  of  a 
few  flecks  or  streaks  of  blood  in  the  sputum  or  it  may  be  so  large  as  to 
cause  death  within  a  few  minutes.  The  sputum  may  be  constantly 
streaked  with  blood  or  pinkish  or  salmon-colored  for  weeks  or  even 
months.  When  the  hemorrhage  consists  of  an  ounce  or  so  of  pure  blood 
the  patient  may  expectorate  dark  clots  or  blood-streaked  sputum  for  a 
few  days.  A  single  hemoptysis  of  this  kind  may  be  the  only  manifes- 
tation of  blood  the  patient  ever  has.  Very  often,  however,  there  are 
recurrences  at  more  or  less  frequent  intervals.  Very  large  hemorrhages 
almost  invariably  occur  in  the  advanced  stages  of  the  disease  when  cavity 
formation  has  taken  place.  As  a  cause  of  death  hemorrhage  is  not  as 
frequent  as  ordinarily  believed.  In  a  study  of  the  cause  of  death  in  136 
cases  I  found  that  a  hemorrhage  was  the  immediate  or  exciting  cause  in 
11.  The  hemorrhage  may  be  so  large  as  to  immediately  cause  death  or 
it  may  give  rise  to  a  widespread  broncho-pneumonia  due  to  insufflation 
of  blood,  which  proves  fatal  in  a  few  days. 

In  the  early  stages  of  the  disease  the  source  of  the  bleeding  is  usually 
from  the  pulmonary  veins  and  the  blood  is  bright  red  in  color  due  to  the 
fact  that  the  pulmonary  veins  carry  arterial  blood.  In  the  moderately 
advanced  and  advanced  cases  the  blood  comes  from  the  pulmonary 
artery  and  is  dark  or  venous  in  color. 

In  many  instances  the  exciting  cause  of  the  bleeding  can  be  determined 
but  in  not  a  few  cases  it  suddenly  appears  without  apparent  cause. 
Recently  I  saw  a  man  who  had  been  discharged  from  the  White  Haven 
Sanatorium  ten  years  ago  with  his  disease  arrested.  During  all  this  time 
he  had  been  in  perfect  health  and  had  worked  at  his  trade  every  day. 
While  walking  along  the  street  he  suddenly  was  seized  with  an  attack  of 
coughing  and  spat  up  a  few  ounces  of  blood.  Aside  from  this  he  had  no 
other  symptoms  and  examination  of  his  chest  shows  no  change  from  that 
noted  ten  years  ago. 

In  many  instances  the  exciting  cause  of  the  bleeding  is  an  acute 
respiratoiy  infection  commonly  manifesting  itself  as  an  ordinary  ''cold." 
In  institutions  it  is  not  at  all  unusual  for  a  number  of  patients  to  have 
attacks  of  hemoptysis  within  a  few  days.  This  epidemic-like  occurrence 
is  undoubtedly  closely  related  to  some  infection.  Some  years  ago  Flick, 
Ravenel  and  Irwin  in  a  study  of  such  cases  were  able  to  show  the  almost 
constant  presence  of  pneumococci  in  the  expectorated  blood. 

As  an  exciting  cause  of  pulmonary  hemorrhage  exertion  of  some 
description  is  usually  considered  as  a  common  factor.  It  is  interesting  to 
note  that  Bang1  in  a  study  of  hemoptysis  found  that  the  hemorrhage  came 
1  Ugeskrift  for  Laeger,  March  23,  1916. 


DISEASES    OF    THE    LUNGS  329 

on  while  the  patients  were  lying  in  bed  or  reclining  in  a  chair  in  69  per  cent, 
of  354  cases.  He  considers  congestion  or  stasis  to  be  the  most  important 
factor.  Thus  50  of  the  patients  had  been  constantly  febrile;  fever  had 
developed  just  prior  to  the  hemorrhage  in  45  and  immediately  afterwards 
in  31;  11  had  been  severely  chilled  and  10  had  received  an  injection  of 
tuberculin. 

Among  women  blood  spitting  may  be  present  just  before  or  during 
the  time  of  the  menstrual  period.  As  the  disease  tends  towards  arrest, 
the  bleeding  gradually  ceases. 

In  cavity  cases  large  hemorrhages  are  usually  the  result  of  rupture  of 
a  pulmonary  blood-vessel.  In  a  large  percentage  of  cavities  there  are 
present  in  the  walls  or  in  the  trabecular  traversing  the  cavity,  blood- 
vessels. Small  aneurismal  dilatations  are  very  commonly  present  in 
the  vessels.  They  may  rupture  through  a  sudden  elevation  of  the  blood- 
pressure  or  the  disease  may  gradually  erode  through  the  arterial  wall. 
In  addition  to  hemorrhages  of  considerable  size  the  sputum  from  cavity 
cases  may  be  pinkish  or  salmon-colored  from  the  admixture  of  blood 
coming  from  ulcerations  in  the  wall  of  the  cavity  and  such  sputum  may  be 
the  precursor  of  a  large  hemorrhage. 

Pain. — Chest  pain  is  one  of  the  common  manifestations  of  tuber- 
culosis. The  character  of  the  pain  varies.  It  is  usually  subjective  but 
may  be  objective  only.  When  objective  it  is  usually  associated  with 
cavity  formation  in  the  lungs  and  is  noted  in  percussing  over  the  site  of 
the  cavity.  Often  there  is  no  subjective  evidence  of  pain  in  spite  of  an 
extensive  pleural  friction  rub.  In  such  cases  pain  can  usually  be  elicited 
by  pressure  with  the  finger  tips  over  the  site  of  the  friction. 

The  character  of  the  subjective  pain  varies  greatly.  It  may  be  sharp 
and  knife-like  as  the  result  of  a  severe  pleurisy  or  in  other  instances  it 
may  consist  of  a  feeling  of  soreness.  Not  uncommonly  the  pain  or 
soreness  is  referred  to  the  region  of  the  shoulder  on  the  affected  side. 
This  fact  should  be  borne  in  mind  as  it  is  commonly  mistaken  for  a  rheu- 
matic manifestation. 

One  of  the  severest  forms  of  pain  occurring  during  the  course  of 
tuberculosis  is  that  sometimes  caused  by  pneumothorax.  The  pain  may 
be  the  only  indication  that  such  an  accident  has  occurred.  The  great 
majority  of  tuberculous  patients  have  some  manifestation  of  chest  pain  at 
one  time  or  another  during  the  course  of  the  disease.  Among  3007  cases 
at  the  Phipps  Institute  chest  pain  was  noted  in  2280  or  75.82  per  cent. 

Vague  and  indefinite  pain  which  has  no  fixed  location  and  no  ap- 
parent anatomical  basis  to  explain  its  cause  is  frequent  in  neurasthenic 
patients.  Among  dispensary  patients  of  Jewish  birth,  it  is  to  be  met 
with  constantly. 

Hoarseness. — Laryngeal  involvement  is  very  common  in  pulmonary 
tuberculosis.  At  one  time  it  was  looked  upon  as  an  absolutely  hopeless 
complication.  This  conception,  however,  took  into  account  only  ad- 
vanced laryngeal  lesions.  We  now  know  that  the  laryngeal  process 
develops  gradually  and  has  an  incipient,  a  moderately  advanced  and  an 
advanced  stage.  Furthermore,  just  as  in  the  lungs,  the  type  of  the  lesion 
has  considerable  bearing  on  the  outcome.  From  the  clinical  standpoint 
the  essential  thing  to  bear  in  mind  is  the  significance  of  hoarseness. 

Hoarseness  as  we  have  alread}-  pointed  out  may  be  temporary  or 
persistent.     When  temporary  it  may  be  constant  for  a  few  weeks  and 


330      DISEASES   OF  THE  BRONCHI,   LUNGS,   PLEURA,   AND   DIAPHRAGM 

gradually  disappear,  especially  if  use  of  the  voice  is  prohibited.  In 
other  instances  it  occurs  only  in  the  morning  on  awakening  or  late  in  the 
day  if  the  voice  has  been  used.  Persistent  hoarseness  is  usually  indica- 
tive of  serious  damage  to  the  larynx;  it  may  be  associated  with  advanced 
pulmonary  lesions  or  may  itself  constitute  the  major  lesion. 

The  great  majority  of  fatal  pulmonary  cases  show  more  or  less  serious 
laryngeal  damage. 

Temporary  hoarseness  was  noted  in  1339  out  of  3007  cases  seen  at 
the  Phipps  Institute  while  persistent  hoarseness  was  noted  in  520  out  of 
4466  cases.  Fetterolf  in  a  clinical  post-mortem  study  of  the  larynx  in 
100  cases  dying  in  the  Phipps  Institute  found  that  it  was  tuberculous  in 
83;  non-tuberculous  in  13;  and  doubtful  in  4. 

Dysphagia. — Difficulty  in  swallowing  is  not  common  in  tuberculous 
patients  except  with  involvement  of  the  pharynx  or  larynx,  usually  the 
latter.  Involvement  of  the  epiglottis  is  especially  liable  to  interfere  with 
swallowing  because  of  pain  which  may  be  so  intense  as  to  prevent  even 
the  swallowing  of  water.  In  some  instances  difficulty  in  swallowing  is 
due  to  interference  with  the  nervous  mechanism  governing  the  larynx. 
This,  however,  is  quite  rare. 

Dyspnea. — Shortness  of  breath  is  a  frequent  complaint  among  those 
suffering  from  tuberculosis.  Curiously  enough  the  degree  of  dyspnea 
bears  very  little  relation  to  the  amount  of  pulmonary  damage.  Little 
or  no  inconvenience  is  experienced  by  some  people,  except  on  exertion, 
in  spite  of  extensive  disease  while  in  others,  with  relatively  little  trouble, 
this  symptom  is  very  troublesome.  While  it  is  undoubtedly  true  that 
the  curtailment  of  the  breathing  space  has  some  influence  on  causing 
shortness  of  breath  there  are  other  factors  which  seem  to  exert  a  more 
marked  influence.  Shortness  of  breath  is  more  apt  to  be  present  if  there 
is  fever  and  is  apparently  dependent  also  on  the  nervous  condition  of  the 
individual.  Patients  who  are  nervous  and  apprehensive  about  their 
condition  are  more  apt  to  suffer  from  shortness  of  breath  and  tachycardia 
than  those  of  a  phlegmatic  temperament.  Immobility  of  the  diaphragm 
is  a  common  cause  of  the  shortness  of  breath.  Some  degree  of  shortness 
of  breath  was  noted  in  80  per  cent,  of  3007  cases  at  the  Phipps  Institute. 
As  a  rule  the  shortness  of  breath  becomes  noticeable  only  on  exertion, 
such  as,  going  upstairs,  climbing  a  hill,  or  walking  fast. 

Physical  Signs. — Before  taking  up  in  detail  the  physical  signs  it  may 
be  well  to  emphasize  the  importance  of  keeping  in  mind  the  morbid 
anatomy,  and  the  symptomatology  of  tuberculosis  in  their  relation  to 
the  physical  findings. 

The  three  factors  involved  in  the  art  of  physical  diagnosis  are  so 
dependent  on  one  another  that  it  is  not  possible  to  say  that  one  is  more 
important  than  the  other.  A  knowledge  of  all  three  is  essential.  It  is 
necessary,  for  instance,  to  know  what  portion  of  the  lung  is  first  involved, 
the  character  of  the  pathological  process  and  how  it  advances  or  retro- 
gresses, as  the  case  may  be.  Knowledge  of  this  sort  and  its  application 
to  physical  signs  is  to  be  learned  largely  in  the  deadhouse,  and  not  at  the 
bedside.  Austin  Flint  expressed  the  importance  of  this  association 
very  clearly  when  he  stated  that:  "The  significance  of  signs  which  repre- 
sent abnormal  physical  conditions  rests  on  the  uniformity  of  their  associa- 
tion with  the  latter — certain  physical  signs  denote  certain  abnormal  condi- 
tions, because  clinical  experience,  inclusive  of  the  study  of  lesions  with 


DISEASES    OF   THE    LUNGS  331 

the  scalpel,  has  sufficiently  established  the  fact."  And  again  he  states 
in  regard  to  physical  signs  that:  "Invaluable  as  they  are,  their  importance 
is  greatly  enhanced  by  association  with  symptoms  and  the  knowledge  of 
pathological  laws.  The  results  of  physical  exploration  alone  frequently 
leave  room  for  doubt  and  liability  to  error,  when  a  due  appreciation  of 
vital  phenomena  and  of  facts  embraced  in  the  natural  history  of  dis- 
eases insures  accuracy  and  positiveness.  An  overweening  confidence  in 
the  former  is  to  be  deprecated,  as  well  as  exclusive  reliance  on  the  latter. 
And,  since  the  practical  discrimination  of  intrathoracic  affections  is 
always  to  be  based  on  the  combined  evidence  afforded  by  these  three 
sources  of  information,  in  treating  of  the  subject  it  is  desirable  that  the 
attention  shall  not  be  limited  to  one  source  to  the  exclusion  of  the  others." 

We  are  largely  indebted  to  the  French  pathologists  for  pointing  out 
the  necessity  of  comparison  of  all  symptoms  of  pulmonary  disease  and 
of  connecting  this  comparison  with  their  succession  in  order.  This  phase 
of  the  subject  was  especially  dealt  with  by  Andral,  and  more  particularly 
by  Louis  in  the  promulgation  of  his  numerical  theory. 

Gerhard  also  emphasized  the  great  importance  of  the  comparison  of 
the  general  symptoms  and  physical  signs.  As  he  points  out,  the  earlier 
writers  on  physical  diagnosis,  especially  Laennec,  were  rather  disposed 
to  separate  physical  from  symptomatic  diagnosis.  And,  although  this 
error  depended  on  the  novelty  of  the  art  and  the  overstrained  efforts  to 
extend  its  application,  it  still  persists,  although  possibly  to  a  less  extent 
than  formerly.  Not  only  are  we  to  avoid  exclusive  reliance  on  the  pres- 
ence or  absence  of  physical  signs,  but  it  is  also  to  be  borne  in  mind  that 
physical  signs,  while  often  indicating  the  extent  and  degree  of  pulmonary 
damage,  convey  no  direct  information  as  to  the  pathological  nature  of 
those  changes. 

As  to  whether  one  shall  take  a  radical  or  a  conservative  view  in  cases 
of  a  doubtful  nature,  there  does  not  seem  to  be,  in  the  writer's  opinion, 
any  room  for  argument.  A  doubtful  case  is  at  best  still  doubtful,  and 
such  being  the  case,  one  should  exercise  every  precaution  to  exclude  the 
presence  of  tuberculosis,  always  bearing  in  mind  that  the  disease  in  its 
very  earliest  stages  is,  as  a  rule,  extremely  amenable  to  treatment.  On 
the  other  hand,  the  more  marked  the  physical  signs,  the  greater  the 
damage  to  the  lung  and  the  more  uncertainty  as  to  whether  the  disease 
can  be  arrested. 

Inspection. — This  method  of  physical  examination  is  too  frequently 
omitted,  or  made  so  hastily  and  cursorily  that  little  or  no  information 
is  obtained.  As  a  matter  of  fact,  inspection  properly  done  yields  more 
valuable  information  than  any  other  procedure  at  our  disposal,  next  to 
auscultation.  And  furthermore,  it  has  this  to  commend  it,  namely,  that 
no  special  training  is  required  and  the  beginner,  providing  he  uses  his 
eyes,  is  as  capable  of  seeing  defects  as  the  trained  observer.  This  is  in 
marked  contrast  to  the  training  necessary  to  educate  the  ear  to  differen- 
tiate sounds,  particularly  those  produced  by  percussion,  the  latter  often 
taking  years  of  practice.  One  who  has  been  taught  to  make  a  proper 
inspection  can  in  the  majority  of  cases  of  tuberculosis,  from  this  method 
alone,  determine  the  side  affected,  and  approximately  the  extent  of  the 
lesion.  As  this  method  takes  no  special  training,  it  is  especially  valuable 
to  the  student  and  to  those  who  see  chest  cases  incidentally^,  and  not 
constantly. 


332      DISEASES   OF   THE  BRONCHI,    LUNGS,    PLEURA,  AND   DIAPHRAGM 

In  order  that  inspection  should  yield  the  best  results  it  is  absolutely- 
essential  that  the  patient  be  stripped  to  the  waist,  and  so  placed  that 
the  parts  under  inspection  are  equally  exposed  to  the  light,  as  an  error 
may  occur  if  one-half  of  the  chest  is  less  well  lighted  than  its  fellow. 

Before  directing  special  attention  to  the  chest  itself  it  is  important 
to  look  for  abnormalities  in  other  regions,  although  the  earlier  the  disease, 
the  less  frequently  do  we  find  anything  of  moment.  In  a  large  number 
of  cases  the  pupils  are  unequal  in  size,  the  dilated  pupil  being  on  the 
affected  side.  Flushing  of  the  cheek  on  the  affected  side  may  be  present 
as  an  early  manifestation,  but  is  more  frequently  encountered  later. 
The  mouth  should  be  examined  at  this  time,  as  a  matter  of  routine,  and 
any  abnormalities  of  the  teeth,  tonsils  or  upper  respiratory  tract  noted. 
Information  of  this  sort,  however,  is  of  value  from  the  standpoint  of 
treatment  rather  than  diagnosis. 

The  thyroid  gland  is  often  enlarged,  although  this  may  be  more 
apparent  than  real  owing  to  emaciation.  Among  2122  patients  seen  at 
the  Phipps  Institute  enlargement  of  the  thyroid  gland  was  noted  in  135 
(6.69  per  cent.) .  In  many  of  these  cases  the  eye  phenomena,  so  commonly 
seen  in  exophthalmic  goitre,  are  also  present. 

_  Inspection  of  the  hands  often  gives  most  valuable  information.  The 
nails  especially  should  be  carefully  examined.  The  most  common  change 
encountered  in  the  nails  is  a  tendency  to  curving,  without  any  associated 
clubbing.  The  nails  not  only  curve  over  the  end  of  the  finger  slightly, 
but  they  are  narrower  from  side  to  side  than  normally.  The  color 
may  be  normal,  or  it  may  be  an  exaggeration  of  the  normal,  whitish- 
pink  color.  While  violet  or  bluish-colored  nails  are  of  frequent  occur- 
rence in  the  advanced  stages  of  the  disease,  they  are  not  usual  in  the  early 
stages;  when  present  at  this  time  they  are  extremely  ominous.  Their 
presence,  in  the  early  stages  of  tuberculosis,  should  cause  one  to  be  very 
guarded  in  predicting  the  outcome,  no  matter  how  slight  the  involvement 
may  seem  from  the  physical  signs,  as  they  usually  indicate  an  especially 
severe  form  of  infection. 

Clubbing  of  the  fingers,  although  usually  stated  to  be  commonly 
associated  with  pulmonary  tuberculosis,  is  as  a  matter  of  fact,  not  fre- 
quent, and  even  when  present,  not  marked.  The  extreme  grades  of 
clubbing  of  the  fingers  occur  for  the  most  part  in  non-tuberculous  affec- 
tions, notably  empyema,  bronchiectasis  and  congenital  heart  disease. 

In  the  early  stages  the  skin  may  present  a  mottled  appearance  indica- 
tive of  a  poor  vasomotor  tone.  Profuse  sweating  either  at  night  or 
after  exertion  is  not  common  at  the  onset  of  the  disease,  but  axillary 
sweating,  often  noted  during  the  examination,  is  sufficiently  frequent  in 
these  cases  to  be  worthy  of  note. 

Taking  up  the  chest  proper,  it  is  usually  best  to  note,  when  visible, 
the  position  of  the  apex  beat  of  the  heart,  as  in  addition  to  disease  of  the 
heart  itself,  the  apex  may  be  displaced  out  of  its  normal  position  as  the 
result  of  disease  of  the  lungs  or  pleura.  An  effusion  displaces  the  heart 
toward  the  opposite  side  while  fibroid  changes  in  the  lung  draw  the 
lung  toward  the  affected  side. 

Coming  now  to  inspection  of  the  chest  with  a  view  of  detecting  pleural 
or  pulmonary  mischief,  it  must  be  borne  in  mind  that  we  are  dealing  with 
comparisons.  In  regard  to  the  shape  of  the  chest,  no  information  of 
importance  is  obtained  in  the  incipient  stage.     The  majority  of  patients 


DISEASES    OF   THE    LUNGS 


333 


at  the  onset  of  the  disease  present  well-shaped  chests,  which  do  not 
present  any  marked  abnormality.  Thus  Pope  and  Brown  found  83 
per  cent,  of  well-formed  chests  in  193  incipient  cases.  The  so-called 
paralytic  thorax,  which  is  sometimes  seen,  is  not  uncommonly  noted  in 
individuals  with  a  marked  hereditary  taint  and  antedates  the  tubercu- 
losis rather  than  being  caused  by  it.  The  paralytic  thorax  is  long  and 
narrow  and  apparently  flattened  in  the  antero-posterior  diameter,  the 
clavicles  and  scapulae  are  prominent,  the  latter  being  tilted  outward  from 
the  chest  and  away  from  the  spine.  The  ribs  are  oblique,  forming  an 
acute  angle  with  the  sternum.     (See  Figs.  13,  24,  31,  35.) 

The  following  points  should  be  noted:     (a)  Whether  the  shoulders 
are  on  a  level;  a  very  early  sign  is  drooping  of  the  shoulder  on  the  affected 


Fig.  251. 


-Shows  drooping  of  the  right  shoulder  and  the  long  line  from  the  neck  to  the 
point  of  the  shoulder. 


side.  In  this  connection,  however,  it  must  be  recalled  that  certain  occu- 
pations, such  as  clerks,  predispose  to  a  faulty  sitting  posture,  which  will 
raise  or  lower  one  shoulder. 

(6)  The  line  from  the  neck  to  the  point  of  the  shoulder.  This  line 
is  normally  slightly  convex,  but  with  beginning  disease  at  one  apex,  it 
tends  to  become  straight  and  also  longer  than  its  fellow,  the  latter  defect 
being  brought  about  by  the  drooping  of  the  shoulder  (Fig.  251). 

(c)  The  degree  of  prominence  of  the  clavicles.  In  most  well-nourished 
women  the  clavicles  are  scarcely,  if  at  all,  visible;  in  men,  on  the  other 
hand,  unless  unusually  fat,  the  clavicles  are  more  or  less  prominent. 

Associated  with  undue  prominence  of  the  clavicle  is  an  exaggeration 
of  the  supraclavicular  fossa.  A  noticeable  amount  of  flattening  may  be 
noted  also  beneath  the  clavicle. 

(d)  Expansion. — Deficient  expansion  of  the  chest  wall  overlying  the 
apex  of  the  lung  is  one  of  the  most  valuable  signs  of  early  tuberculosis 
which  we  possess.  It  is  especially  to  be  looked  for  toward  jthe  outer 
border  of  the  lung,  just  beneath  the  clavicle.     In  this  situation  the 


334      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND  DIAPHRAGM 

chest  wall  normally  balloons  out  quite  markedly.  If,  however,  there 
exists  an  infiltration  of  tubercles  at  or  near  the  apex,  the  underlying  lung 
does  not  expand  as  fully  as  its  fellow,  or  if  the  expansion  is  equal  on  both 
sides  the  affected  side  tends  to  lag  behind  slightly,  especially  at  the 
beginning  of  the  inspiratory  period. 

Inspection  of  the  apices  for  the  purpose  of  determining  the  degree 
of  expansion  yields  the  best  results,  if  but  one  apex  is  involved.  If 
there  exists  disease  at  the  summit  of  both  lungs  the  value  of  comparison 
is  thus  lost,  and  one  may  be  unable  to  come  to  any  definite  conclusion 
from  this  method  alone.  Two  other  methods  of  determining  slight 
amounts  of  retraction  on  the  affected  side  are  available,  namely,  palpation 
and  mensuration,  both  of  which  will  be  described  in  detail  later. 

Inspection  of  the  chest  posteriorly.  In  the  early  stages  of  tubercu- 
losis the  amount  of  information  gained  from  the  posterior  view  of  the 
chest  is  slight  compared  to  what  can  be  learned  from  the  anterior  view. 
A  very  common  occurrence  in  tuberculous  subjects  is  the  presence  of 
fine  venules  in  the  region  of  the  nape  of  the  neck.  These  small  veins 
may  be  bluish  or  purplish  in  color.  They  have  been  cited  as  an  evidence 
of  the  existence  of  pulmonary  tuberculosis,  but  are  so  frequently 
encountered  as  to  be  of  little  value  as  a  diagnostic  sign. 

Owing  to  the  interposition  of  the  scapular  muscles  and  the  ribs  little 
can  be  noted  as  to  expansion  in  the  upper  part  of  the  chest.  At  the  bases, 
however,  expansion  can  be  determined  in  the  same  manner  as  over  the 
apices  anteriorly.  The  most  noticeable  finding  is  the  presence  of  varying 
degrees  of  atrophy  of  the  muscles  in  the  supraspinous  fossa.  If  the  arms 
are  allowed  to  hang  naturally  at  the  sides,  the  angle  of  the  scapula  on  the 
affected  side  may  tip  backward  slightly  more  than  its  fellow.  This 
tendency  to  " winged  scapulae"  becomes  much  more  marked  as  the 
disease  progresses. 

Slight  degrees  of  scoliosis  may  be  present.  Litten's  sign  may  be 
present  (see  Part  I,  p.  28).  The  sign  is  not  often  employed  as  there  is 
another  and  easier  method  of  determining  the  mobility  of  the  lower  part 
of  the  lung,  namely,  by  percussing  the  lower  border  of  the  lung  during 
forced  expiration  and  inspiration.  The  fluoroscope  may  be  employed 
also. 

Palpation. — Tactile  fremitus  is  a  sign  of  comparatively  little  value  in 
incipient  tuberculosis,  as  the  amount  of  infiltration  in  the  underlying 
lung  is  usually  too  slight  to  produce  much  exaggeration  over  the  normal. 
The  normal  discrepancy  between  the  two  apices  has  already  been  alluded 
to  (see  p.  73). 

Pottenger  has  called  attention  to  rigidity  of  the  muscles  over  the 
affected  area.  Recently  Galecki1  reports  on  finding  this  sign  present  in 
93  per  cent,  of  recent  cases  and  not  at  all  in  cases  with  a  healed  lesion. 
The  sign  is  elicited  by  light  touch  palpation.  This  sign  is  not  to  be  con- 
fused with  myoidema.  The  latter  term  is  applied  to  a  local  contraction 
of  the  muscle,  produced  by  direct  percussion,  and  causing  a  nodular  swell- 
ing, which  arises  immediately  after  percussion,  lasts  a  second  or  two, 
and  then  gradually  disappears.  It  may  be  produced  two  or  three  times 
and  then  cease  to  appear.  It  is  best  seen  in  the  pectoralis  major  muscle. 
Although  this  phenomenon  is  commonly  encountered  in  tuberculosis, 
it  is  not  peculiar  to  the  disease. 

1  Beitrdge  Zur  Klin.  d.  Tuberculose,  1914,  xxx,  No.  3. 


DISEASES    OF   THE    LUNGS  335 

Palpation,  however,  is  an  invaluable  method,  for  determining  the 
amount  of  expansion  at  the  apices  in  those  instances  where  the  difference 
between  the  two  sides  is  slight  and  one  is  in  doubt  from  inspection  alone. 
In  determining  the  degree  of  expansion  over  the  apices  anteriorly  by 
means  of  palpation,  one  of  two  procedures  may  be  followed.  The 
examiner  sits  squarely  in  front  of  the  patient  and  places  one  hand  in  the 
same  relative  position  beneath  each  clavicle;  he  should  then  close  his 
eyes,  or  turn  his  head  aside.  In  this  way  even  the  very  slightest  variation 
may  be  noted.  Or  the  examiner  can  watch  his  two  hands  and  determine 
which  moves  the  most.  The  former  is  by  far  the  more  delicate  method. 
The  value  of  the  sign  is  enhanced  by  the  readiness  with  which  it  is 
elicited.  Students  with  but  a  rudimentary  knowledge  of  physical  diag- 
nosis can  readily  detect  a  slight  difference  between  the  two  apices  when 
the  other  signs,  indicative  of  a  lesion,  are  too  vague  to  be  appreciated  by 
an  untrained  observer.  In  the  incipient  stage  palpation  is  not  apt  to 
reveal  abnormalities  in  portions  of  the  chest  other  than  one  or  the  other 
apex. 

Mensuration  is  the  least  used  of  the  various  procedures  of  physical 
diagnosis.  At  one  time  a  great  deal  of  stress  was  laid  on  the  degree  of 
expansion  of  the  chest,  good  expansive  power  being  looked  upon  as  in- 
dicating freedom  from  thoracic  disease;  and  insurance  companies  still 
insist  on  a  record  of  the  difference  between  expiration  and  deep  inspira- 
tion. In  the  absence  of  more  convincing  signs  it  is  doubtful  whether 
any  importance  can  be  attached  to  a  degree  of  expansion  below  the 
normal  (approximately  2}^  inches) ,  if  this  is  the  only  evidence  obtainable. 

A  more  useful  method  of  employing  mensuration  is  by  means  of  the 
lead  tape  cyrtometer.  This  method  is  too  little  used.  While  it  is  valuable 
for  diagnostic  purposes,  its  greatest  usefulness  is  in  depicting  the  changes 
in  the  contour  of  the  chest  as  the  disease  progresses,  either  to  a  favorable 
or  an  unfavorable  termination.  The  technique  of  the  method  is  readily 
acquired  with  a  little  practice.  The  lead  cyrtometer  consists  of  a  piece 
of  sheet  lead,  ^f  q  inch  thick,  ^  inch  wide  and  26  inches  long.  It  should 
be  covered  with  thin  calfskin.  In  addition  there  is  required  a  pair  of 
obstetrical  calipers  capable  of  opening  at  least  12  inches.  The  first  step 
is  to  obtain  the  antero-posterior  diameter  of  the  chest.  Minor  recom- 
mends for  the  two  fixed  points,  the  middle  of  the  sternum  at  the  level  of 
the  fourth  costal  cartilage  in  front,  and  the  eighth  dorsal  spine  posteriorly. 
The  latter  is  a  little  below  the  level  of  the  inferior  angles  of  the  scapulae. 
Having,  with  the  calipers,  ascertained  the  depth  of  the  chest  between 
the  above-mentioned  points  the  distance  is  marked  on  a  sheet  of  paper, 
capable  of  receiving  the  tracing  of  a  chest  12  inches  in  its  antero-posterior 
diameter  and  16  inches  in  its  lateral  diameter. 

Each  half  of  the  chest  is  taken  separately.  With  the  eighth  dorsal 
spine  as  the  fixed  point,  one  end  of  the  tape  is  firmly  held  so  that  it  will 
not  slip  and  is  then  brought  around  to  the  anterior  fixed  point.  The  tape 
should  be  firmly  applied  so  that  it  fits  snugly.  In  crossing  the  axillary 
space  care  must  be  taken  to  mould  the  tape  to  the  chest  wall,  otherwise 
this  space  is  apt  to  be  bridged.  The  anterior  point  can  be  marked  by 
indenting  the  leather  with  the  finger  nail.  The  tape  is  then  carefully 
removed  and  the  two  ends  placed  over  the  marks  indicated  on  the  paper 
by  the  calipers.  By  means  of  a  pencil  the  perimeter  is  then  traced  on  the 
paper.     The  left  side  is  similarly  taken  (Figs.  252,  253  and  25-f). 


336      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

By  using  different  colored  pencils  at  each  subsequent  tracing,  one 
obtains  an  excellent  picture  of  the  contour  of  the  chest.  Even  in  very 
early  cases  there  is  a  slight  amount  of  shrinkage  on  the  affected  side,  and 
the  greater  the  amount  of  disease  present  the  greater,  as  a  rule,  is  the 
degree   of   retraction.     As   the    case   progresses    toward    recovery    the 


A 
Fig.  252. — Slight  retraction  of  right  side.     Lesion  at  right  apex. 


A 

Fig.  253. — Slight  retraction  of  left  side.     Lesion  at  left  apex. 

P 


A 

Fig.  254. — Advanced  bilateral  disease.     Marked  retraction  of  right  side. 

affected  side  tends  to  fill  out  so  that  eventually  discrepancies  between  the 
two  sides  disappear.  In  some  early  cases  with  a  marked  degree  of 
shrinkages,  the  reexpansion  is  quite  rapid.  On  the  other  hand,  if  the 
disease  advances,  the  affected  side  shows  an  increased  amount  of  re- 
traction, and  with  involvement  of  the  sound  side  evidences  of  shrinkage 
will  likewise  appear.     Minor  states  that  the  increase  of  the  perimeter 


DISEASES    OF   THE    LUNGS  337 

takes  place  on  the  unaffected  side  first  as  a  result  of  the  compensatory 
action  of  the  sound  lung,  and  that  the  increase  of  the  affected  side  gener- 
ally follows  the  increase  of  the  unaffected  side.  The  increase  can  be  in 
breadth  or  depth;  the  latter  is  of  more  significance,  however,  as  the  trac- 
ing of  the  former  may  be  affected  by  an  increase  in  the  amount  of  fat 
and  muscle,  while  the  latter  being  measured  between  two  bony  points  is 
not  so  affected.  Thus  it  can  be  seen  that  the  method  is  a  valuable  diag- 
nostic, as  well  as  a  prognostic  aid.  One  precaution  should  be  kept  in 
mind,  namely,  as  to  whether  the  individual  is  right-handed  or  left-handed. 
Percussion. — Before  undertaking  to  describe  the  percussion  changes 
in  early  tuberculosis,  it  is  necessary  to  emphasize  several  important  facts. 

1.  There  is  a  normal  discrepancy  between  the  percussion  notes  of 
the  two  apices.  This  has  been  recognized  for  many  years,  but  advantage 
is  not  always  taken  of  the  knowledge.  The  note  on  the  right  side  is 
normally  a  little  higher  in  pitch  and  a  little  less  resonant  than  the  note  on 
the  left  side.  Flint  described  the  note  on  the  right  side  as  vesiculo- 
tympanitic without,  however,  advancing  any  reason  for  the  change. 
Recently  Fetterolf  and  Norris  have  given  a  satisfactory  explanation  of 
the  difference.  Their  study,  from  both  the  clinical  and  anatomical  stand- 
points, shows  quite  clearly  that  the  right  apex  is  smaller  than  the  left 
(see  Figs.  62,  63,  64,  76  and  77)  and  that  furthermore  the  position  of  the 
bloocl-vsesels  on  the  right  side  tend  to  diminish  the  resonance.  The  close 
approximation  of  the  right  apex  to  the  trachea  (see  Figs.  49,  75,  95  and 
104),  the  latter  giving  a  tympanitic  note,  thus  tends  to  raise  the  pitch 
of  the  percussion  note;  the  left  apex,  being  larger  and  having  large  blood- 
vessels and  areolar  tissue  interposed  between  it  and  the  trachea,  gives  a 
pure  resonant  note. 

2.  One  of  the  difficulties  the  beginner  has  in  percussing  the  apices  is 
that  to  his  ear  the  note  is  frequently  impaired.  The  real  difficulty, 
however,  is  that  the  note  is  less  intense  in  this  region  owing  to  the  small 
amount  of  lung  tissue  at  the  apex  as  compared  to  the  base,  and  also  be- 
cause of  the  distance  of  the  lung  from  the  surface  over  which  the  per- 
cussion is  being  applied.  These  differences  apply  to  the  posterior  aspect 
of  the  apex,  and  to  a  less  extent,  the  area  above  the  clavicle.  Anteriorly 
beneath  the  clavicle  the  pulmonary  tissue,  lies  immediately  beneath  the 
chest  wall  so  that  the  note  is  usually  intense,  and  on  the  left  side  typically 
resonant  (see  Figs.  260,  261,  and  262). 

3.  Keeping  in  mind  this  normal  difference,  it  must  be  remembered 
again  that  we  are  dealing  with  comparisons,  and  inasmuch  as  the  changes 
are  at  best  slight,  each  side  must  be  compared  carefully  with  the  other. 
If  slight  changes  exist  at  the  summit  of  both  lungs  it  is  probable  that  very 
little  definite  information  will  be  forthcoming  from  percussion. 

Percussion  of  the  apices  in  a  case  of  suspected  incipient  tuberculosis 
is  a  procedure  that  requires  a  well-trained  ear,  and  not  a  little  experience. 
The  change  from  the  normal  is  usually  so  slight  that  for  the  beginner  the 
method  is  the  least  fruitful  of  results;  and  even  the  experienced  observer 
is,  in  doubtful  cases,  apt  to  be  influenced  in  his  interpretation  by  the 
presence  or  absence  of  symptoms,  or  other  associated  physical  signs. 
The  detection  of  slight  changes  at  the  apex  is  facilitated  by  marking  with 
a  skin  pencil  the  borders  of  what  is  known  as  "  Kronig's  isthnius."  This 
is  a  band  of  resonance  which  crosses  the  shoulder  (Figs.  255  and  256).' 
Its  narrowest  point  is  at  the  top  of  the  shoulder,  and  in  both  front 


338      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,    AND    DIAPHRAGM 

and  back  it  widens  out  to  meet  the  extended  areas  of  resonance  beneath 
the  clavicle  and  supraspinous  fossa.  The  value  of  this  sign  arises  because 
of  the  well-known  tendency  of  the  lung  with  a  developing  tuberculous 
focus  to  shrink,  either  as  the  result  of  fibrosis,  or  of  lessened  functional 
activity. 

In  mapping  out  the  "isthmus"  it  is  well  to  begin  the  percussion  well 
up  the  side  of  the  neck  and  gradually  come  downward  until  a  change 
from  non-resonance  to  resonance  is  noted.  This  point  is  marked  with 
the  pencil  and  by  working  either  forward  or  backward  the  inner  line  is 
traced  out.  The  outer  line  is  mapped  out  similarly  by  approaching  the 
resonant  area  from  the  point  of  the  shoulder.  The  inner  line,  except  at 
the  inner  anterior  extremity,  is  concave  and  runs  downward  and  for- 
ward, ending  just  a  little  outside  the  sterno-clavicular  joint.     Posteriorly 


Fig.   255. — Kronig's  isthmus. 
Normal  anterior  view. 


Fig!  256. — Kronig's  isthmus. 
Normal  posterior  view. 


the  inner  line  inclines  toward  the  spinal  column;  at  the  level  of  the  second 
dorsal  vertebra  it  continues  parallel  with  the  spinal  column,  at  a  distance 
of  about  }/%  inch. 

The  outer  line,  anteriorly,  runs  downward  and  outward,  ending 
at  the  junction  of  the  outer  and  middle  third  of  the  clavicle.  Posteriorly 
it  runs  downward  to  about  the  middle  of  the  spine  of  the  scapula. 

The  value  of  this  procedure  lies  in  the  fact  that  while  one  may  be  in 
doubt  as  to  the  quality  of  the  note,  if  percussion  is  made  directly  over 
the  situation  of  normal  resonance,  one  is  less  likely  to  err  if  the  normal 
area  is  approached  from  non-resonant  parts,  such  as  the  neck  or  shoul- 
der. One  quickly  learns  to  appreciate  what  the  normal  width  of  the 
isthmus  should  be,  and  if  this  becomes  narrower  it  is  an  indication  of 
trouble  in  the  underlying  apex.  If  but  one  side  is  diseased,  the  affected 
side  will  show  a  much  narrower  "isthmus"  than  the  healthy  side  (Figs. 
257  and  258).  As  the  disease  becomes  more  extensive  at  the  apex  the 
two  lines  of  the  "isthmus"  tend  to  become  closer  and  closer  "until 
finally  in  the  advanced  case  no  semblance  of  resonance  remains. 

Some  observers  have  laid  stress  on  direct  percussion  of  the  clavicles 
without  the  intervention  of  a  plexor,  the  claim  being  made  that  at  times, 


DISEASES    OF   THE    LUNGS 


339 


a  small  area  of  impairment  can  be  detected  that  would  otherwise  escape 
detection.  Such  instances  may  occur,  but  they  are  far  from  being 
common. 

Having  outlined  the  apices  the  percussion  should  be  continued  down- 
ward until  the  base  of  the  lung  is  reached.  Even  in  incipient  cases  it 
will  usually  be  found  that  the  resonance  does  not  extend  quite  so  low  on 
the  affected  as  on  the  unaffected  side  after  deep  inspiration  (see  Fig.  259) . 
It  will  be  recalled  that  mensuration  shows  some  diminution  in  the  size 
of  the  affected  side.  Furthermore,  it  has  been  shown  by  fluoroscopic 
examinations  that  the  descent  of  the  diaphragm  on  the  affected  side  is 
usually  diminished.  This  is  known  as  Williams'  early  diaphragmatic 
sign  (see  p.  596).  These  observations  indicate  that  the  lung,  even  when 
the  seat  of  a  small  amount  of  disease,  functionates  less  freely  than  the 


Fig.  257. — Kronig's  isthmus  Normal 
on  left  side.  Narrowed  on  right  side  due 
to  tuberculosis  of  right  apex. 


'Fig.  258. — Kronig's  isthmus.     Both  sides 
narrow  due  to  bilateral  tuberculosis. 


unaffected  lung,  or  that  the  unaffected  lung  is  functionating  more  than 
the  diseased  one.  Whichever  is  the  correct  explanation,  the  fact  remains 
that  the  resonant  note  is  apt  to  stop  at  a  higher  level  on  the  affected, 
than  the  unaffected  side. 

With  ordinary  quiet  breathing  the  bases  of  the  lungs  extend  to  the 
level  of  the  tenth  dorsal  vertebra;  the  complementary  space  of  the  pleural 
cavity,  however,  extends  to  the  level  of  the  twelfth  dorsal  vertebra. 
On  deep  inspiration  the  lung  can  be  made  to  expand  for  an  inch  or  more 
below  the  level  of  the  tenth  dorsal  vertebra,  providing  it  or  the  pleura 
is  free  from  disease.  If,  however,  the  lung  is  much  diseased,  or  the 
pleural  cavity  is  obliterated,  or  the  diaphragm  is  immobile,  the  base 
line  on  the  affected  side  remains  stationary. 

Having  marked  out  the  borders  of  the  lung,  the  heart  and  viscera 
in  relationship  to  the  lungs  should  be  outlined. 

Auscultation. — The  fact  that  there  normally  exists  a  difference  be- 
tween the  right  and  left  apex  has  already  been  alluded  to  (se"e  p.  73). 
Nothing  further  need  be  said  except  to  emphasize  the  importance    of 


340      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND  DIAPHRAGM 

bearing  this  in  mind.  One  other  fact  should  be  mentioned,  namely,  the 
relative  importance  of  the  different  steps  taken  to  determine  whether  one 
or  the  other  apex  is  the  seat  of  tuberculous  disease.  That  auscultation 
is  the  most  important  means  at  our  disposal  for  the  detection  of  intra- 
thoracic disease,  there  can  be  no  doubt.  On  the  other  hand,  it  is  equally 
true  that  in  those  instances  in  which  the  pulmonary  damage  is  slight  aus- 
cultation alone,  valuable  as  it  is,  will  frequently  fail.  The  recognition  of 
true  incipient  tuberculosis  cannot  be  accomplished  except  by  a  careful  con- 
sideration of  the  facts  revealed  in  the  history,  and  a  proper  estimation  of 
the  slight  deviation  from  normal  as  revealed  by  inspection,  palpation,  men- 
suration and  percussion.     Even  a  skilled  auscultator  would  often  be  in 


Fig.  259. — Restriction  of  motion  at  base  of  left  lung.     Lesion  at  left  apex. 

doubt  as  to  the  presence  of  a  slight  tuberculous  deposit  if  he  relied  on  aus- 
cultation alone.  The  question  as  to  whether  suspicious  breath  sounds 
may  be  considered  normal  or  abnormal  not  infrequently  hinges  on  the 
character  of  the  information  obtained  in  the  history  and  by  the  other 
methods  of  physical  exploration.  This  digression  has  seemed  necessary 
because  of  the  absolute  reliance  so  many  physicians  place  on  auscultation 
alone. 

Granular  Breathing. — This  type  of  breathing,  which  owes  its  impor- 
tance as  an  early  diagnostic  sign  to  Grancher,  and  in  this  country  to 
Minor,  is  now  regarded  as  the  earliest  manifestation  of  the  auscultatory 
changes  in  pulmonary  tuberculosis.  While  readily  recognized  after 
one  has  heard  it  a  few  times,  it  is  a  sound  not  easily  described  by  words. 
Granular  breathing  is  a  rough  or  sputtering  type  of  breathing.  Turban 
has  likened  this  type  of  breathing  to  the  rapid  succession  of  minute 


DISEASES    OF    THE    LUNGS  3-41 

explosions;  Minor  to  "a  succession  of  very  short  sounds,  as  though  small, 
soft  granules  of  fine,  wet  sago  were  being  rolled  over  each  other."  Per- 
haps the  clearest  description  is  that  it  suggests  the  coexistence  of  rales, 
and  yet,  just  as  the  listener  fully  expects  to  hear  fine  rales  at  the  end  of 
inspiration,  the  inspiratory  phase  ceases.  This  type  of  breathing  has 
been  described  as  being  due  to  slight  narrowing  or  uneven  surface  of  the 
bronchioles,  or  to  a  rapid  interruption  of  the  air  entering  the  alveoli 
about  the  tuberculous  deposit.  The  following  seems  to  us  a  more 
plausible  explanation.  It  should  be  recalled  that  in  the  early  stages  of 
pulmonary  tuberculosis  there  is  a  considerable  amount  of  relaxation  and 
collapse,  or  partial  collapse  of  the  vesicles  immediately  around  the  tuber- 
cles. As  the  air  forces  its  way  into  these  partially  collapsed  vesicles  they 
expand  independently  instead  of  synchronously.  This  imparts  to  the 
inspiratory  murmur  a  jerky  sound  and  also  gives  the  impression  of  crepi- 
tation due  to  the  separation  of  the  slightly  moistened  wall  of  the  air 
vesicles. 

Feeble  Breathing. — Next  in  importance  to  granular  breathing  is 
slight  enfeeblement  of  the  respiratory  murmur.  This  type  needs  no 
special  description.  If  on  comparing  the  two  apices  the  breath  sounds 
are  less  intense  on  one  side  than  the  other,  the  fact  is  significant.  It 
is  usually  taught  that  enfeebled  breathing  to  be  of  significance  as  an  early 
sign  in  tuberculosis  must  be  limited  to  the  apex.  It  has  been  our  experi- 
ence, however,  that  the  breath  sounds  all  over  the  affected  lung,  even 
with  veiy  slight  apical  signs,  are  not  infrequently  less  intense  than  over 
the  affected  side.  This  is  after  all  not  surprising,  when  we  recall  that 
mensuration  shows  a  diminution  of  the  affected  side  and  the  fluoroscope 
a  heightened  diaphragm. 

Prolonged  Expiration. — Prolonged  expiration,  although  not  the  earli- 
est change  from  the  normal  in  the  breath  sounds,  is  the  most  usual  find- 
ing, as  the  two  earlier  changes  described  above  often  escape  detection. 
The  respiratory  murmur  in  this  type  of  breathing  may  be  harsh  or 
slightly  suppressed,  but  in  either  instance  the  characteristic  feature  is 
the  prolonged,  high-pitched,  bronchial  quality  of  the  expiration.  Heard 
at  the  left  apex,  one  is  rarely  in  doubt  as  to  its  significance;  when  con- 
fined to  the  right  side,  there  is  apt  to  be  a  certain  amount  of  question 
as  to  whether  we  are  dealing  with  normal  or  pathological  broncho-vesi- 
cular breathing.  While  in  every  normal  chest  there  is  more  or  less 
marked  broncho-vesicular  breathing  at  the  right  apex,  there  is  no  definite 
standard  and  the  question  of  whether  it  is  pathological  or  not  is  usually 
settled  by  the  presence  or  absence  of  collateral  evidence.  In  children 
especially  there  is  a  strong  tendency  towards  exaggeration  of  the  normal 
signs  at  the  right  apex,  and  not  infrequently  children  are  said  to  be  tuber- 
culous, because  of  the  strong  transmission  of  both  the  spoken  and  whis- 
pered voice  and  the  prolonged  blowing  character  of  expiration. 

Cog-wheel  or  Wavy  Breathing. — Cog-wheel  or  wavy  breathing  has  been 
described  as  an  evidence  of  incipient  tuberculosis,  but  the  best  authorities 
now  are  agreed  that  it  can  no  longer  be  considered  of  importance  as  an 
early  sign.  As  the  name  indicates  it  is  an  interrupted  tj^pe  of  breathing. 
The  inspiratory  phase  is  the  one  commonly  subject  to  the  interruptions; 
rarely  the  expiratorj^.  It  may  occur  in  a  patient  suffering  from  the  pain 
of  acute  pleurisy,  or  in  nervous  or  chilly  individuals.  In  tuberculous 
subjects  it  is  usually  heard  over  areas  which  divide  healthy  frofh  diseased 


342      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

tissue.  Cog-wheel  breathing  is  not  to  be  confounded  with  the  cardio- 
inspiratory  murmur  of  which  we  will  speak  presently. 

Vocal  Resonance. — The  alterations  in  the  voice  sounds  are  not  of  great 
value  in  early  tuberculosis,  as  the  deviation  from  the  normal  may  not  be 
sufficient  to  be  appreciated.  The  whispered  voice  is  normally  heard  with 
distinctness  over  the  second  costal  cartilage  on  the  right  side,  and  poste- 
riorly in  the  interscapular  regions.  In  many  chests  it  is  indistinctly 
heard  also  over  the  extreme  right  apex  anteriorly  and  posteriorly.  In- 
distinct whispering  pectoriloquy  in  the  latter  situation  is  of  no  significance 
without  collateral  evidence.  As  an  indication  of  infiltration  the  whis- 
pered voice  is  subject  to  the  same  rule  as  the  spoken  voice. 

Rales. — I  have  already  pointed  out  that  in  the  earliest  change  of  the 
breath  sounds  (that  is  the  " granular  breathing")  one  gets  the  impression 
that  rales  are  about  to  be  heard,  but  as  a  matter  of  fact  are  not.  In  true 
incipient  tuberculosis,  no  matter  what  the  type  of  breathing  may  be,  rales 
are  not  heard  with  ordinary  quiet  breathing.  If,  however,  a  deep  in- 
spiration is  taken,  fine,  dry  crackles  may  be  elicited  above  or  just  below 
the  clavicle,  or  above  the  spine  of  the  scapula,  posteriorly  on  the  affected 
side. 

An  invaluable  procedure  for  bringing  out  these  rales  is  after  auscultat- 
ing the  chest,  while  the  patient  is  breathing  quietly  through  the  mouth, 
to  have  him  give  a  short  cough,  followed  by  a  moderately  deep  inspiration. 
This  is  repeated  first  on  one  side,  then  the  other  until  the  entire  chest  has 
been  gone  over.  In  this  way  small,  localized  areas  containing  these  fine 
rales  are  detected  which  would  otherwise  escape  observation.  If  crackles 
are  confined  to  an  apex  and  do  not  disappear  after  deep  breathing  or 
coughing,  they  are  the  strongest  kind  of  evidence  of  the  existence  of  a 
pulmonary  tuberculosis.  In  other  situations  they  are  of  less  importance 
as  a  diagnostic  sign  of  tuberculosis. 

Rales  that  are  heard  with  ordinary  quiet  breathing  are  somewhat 
coarser,  and  in  addition  give  the  impression  of  moisture.  Rales  heard 
under  these  circumstances  are  not  evidence  of  incipiency,  but  indicate 
that  the  disease  has  probably  passed  that  stage.  This  is  true  also  of  the 
larger  moist  rales  (the  so-called  mucous  click,  etc.)  even  though  limited 
to  one  apex. 

Cardiac  Phenomena  Occurring  in  Tuberculosis. — Most  of  the  abnormal 
signs  of  cardiac  origin  in  tuberculosis  manifest  themselves  in  the  second 
and  third  stages  of  the  disease. 

The  heart  sounds  are  at  times  unduly  transmitted  toward  the  affected 
apex,  even  in  the  incipient  stage,  and  the  denser  the  infiltration  the  more 
intense  do  the  heart  sounds  become. 

Cardio-respiratory  murmurs  are  common  in  tuberculous  subjects,  and 
while  they  have  lost  much  of  the  diagnostic  significance  attached  to  them 
by  the  older  clinicians,  it  is  surprising  how  frequently  they  are  encountered 
in  tuberculous  patients.  They  are  as  a  rule  associated  with  a  rapid 
cardiac  action  (see  p.  247). 

While  the  cardio-respiratory  murmur  may  be  heard  in  the  incipient 
stage,  it  is  more  commonly  encountered  in  the  moderately  advanced 
stages  of  the  disease.  It  is  also  encountered  in  individuals  with  an  old 
healed  lesion  at  one  or  the  other  apex.  In  the  same  category  may  be 
placed  systolic  murmurs  heard  in  the  subclavian  arteries. 

The  frequency  of  the  heart's  action  is  not  greatly  accelerated  in  the 


DISEASES    OF   THE    LUNGS  343 

early  stages;  if  so,  it  is  an  indication  of  marked  toxemia.  A  single 
office  observation  as  to  the  frequency  of  the  heart's  action  is  untrust- 
worthy because  of  the  nervousness  and  excitement  often  incident  to  the 
examination.  To  be  of  value  the  pulse  rate  must  be  observed  with  the 
patient  at  rest  for  a  number  of  days.  As  the  disease  progresses  the 
heart's  action  almost  invariably  increases  in  frequency.  With  the  de- 
velopment of  tachycardia,  even  moderately  severe,  reduplication  of  the 
heart  sounds  is  frequent,  particularly  the  second  pulmonic;  less  fre- 
quently the  first  sound  at  the  apex.  With  extensive  disease  of  the  left 
lung,  retraction  of  its  anterior  border  is  common.  This  results  in  visible 
pulsation  of  the  heart  in  the  region  of  the  second  costal  cartilage  on  the 
left  side. 

At  one  time  it  was  currently  believed  that  an  individual  who  suf- 
fered from  organic  heart  disease  was  not  apt  to  become  tuberculous. 
As  Norris  pointed  out  some  years  ago,  there  is  no  support  for  this  theory, 
and  one  is  apt  to  encounter  an  associated  organic  lesion  of  the  heart  as 
frequently  in  tuberculosis  as  in  any  other  disease.  In  addition  to  organic 
murmurs,  accidental  murmurs  of  unknown  origin  are  frequent,  particu- 
larly in  the  latter  stages  of  the  disease.  Functional  murmurs,  systolic 
in  time,  are  of  not  infrequent  occurrence  at  the  apex,  but  by  far  the  most 
frequent  murmur  of  this  type  is  a  systolic  murmur  heard  at  the  base 
of  the  heart,  at  or  near  the  second  pulmonic  area. 

Physical  Signs  in  the  Second  or  Moderately  Advanced  Stage. — In- 
spection:— When  the  disease  has  progressed  sufficiently  to  be  designated 
moderately  advanced,  the  general  health  of  the  patient  begins  to  show 
impairment  (see  Fig.  230).  The  loss  of  weight  is  apt  to  be  noticeable 
and  the  muscles  present  a  flabby  condition.  Slight  flushing  of  the  cheek 
on  the  affected  side  is  frequently  noted  and  this  is  in  striking  contrast 
to  the  anemia. 

Skin  eruptions  which  are  not  uncommon  in  the  third  or  advanced 
stage  may  make  their  appearance  during  the  second  stage.  The  com- 
monest of  these  eruptions  is  pityriasis  versicolor  caused  by  the  micro- 
sporon  furfur. 

As  to  the  chest  itself  the  affected  side  shows  more  marked  evidence 
of  shrinkage.  The  clavicle  is  more  prominent;  the  fossa  above  the 
clavicle  is  deeper  and  flattening  beneath  the  clavicle  more  noticeable. 
Diminution  Of  expansion  which,  in  the  incipient  stage,  is  not  always 
apparent  on  inspection,  becomes  readily  so  in  this  stage. 

Some  atrophy  of  the  muscles  overlying  the  affected  apex  is  apt  to 
make  its  appearance  at  this  time.  Including  all  types  of  cases  atrophy 
of  the  muscles  was  noted  at  the  Phipps  Institute  in  1325  cases  out  of  4343 
— $31  on  the  right  side  and  394  on  the  left.  In  women  the  breast  on  the 
affected  side  may  be  distinctly  smaller  than  that  on  the  opposite  side. 

Varying  degrees  of  spinal  curvature  are  also  of  frequent  occurrence 
and  the  more  extensive  the  disease  the  more  marked  does  this  tendency 
become.  Spinal  curvature  was  recorded  as  having  been  present  in  968 
out  of  3436  cases  of  all  types  at  the  Phipps  Institute. 

The  heart  is  not  apt  to  be  noticeably  displaced  at  this  time. 

Palpation. — This  confirms  the  diminished  respiratory  movement 
over  the  affected  area  already  noted  on  inspection.  The  tactile  fremitus 
is  usually  exaggerated  but  may  show  no  appreciable  changer.. 

Percussion. — While  in  the  incipient  stage  one  is  often  in  doubt  as  to 
whether  the  percussion  note  deviates  from  the  normal;  this  is  rarely  so 


344      DISEASES   OF   THE  BRONCHI,    LUNGS,    PLEURA,    AND   DIAPHRAGM 

when  the  infiltration  has  become  more  dense  and  more  tissue  is  involved. 
In  the  majority  of  instances  the  percussion  note  is  not  entirely  devoid  of 
resonance  because  the  tuberculous  infiltration  is  rarely  massive.  Patches 
of  air-bearing  tissue  still  exist  about  the  tubercles  and  for  this  reason 
varying  degrees  of  pulmonary  resonance  persist.  In  some  cases  a  tym- 
panitic note  is  obtained  as  the  result  of  cavity  formation.  This,  however, 
is  usually  a  manifestation  of  advanced  disease,  the  signs  of  which  will  be 
considered  in  detail  later. 

Kronig's  isthmus  becomes  narrower  in  the  second  stage  and  the  im- 
paired percussion  note  may  extend  as  low  as  the  third  or  fourth  rib  (see 
Fig.  258).  By  the  time  the  infiltration  has  become  marked  at  the  apex 
and  shrinkage  of  the  affected  side  is  apparent  the  percussion  note  at  the 
base  will  be  found  to  be  on  a  higher  level  than  the  sound  side.  With  the 
disease  advanced  to  the  second  stage  at  one  apex  there  may  be  signs 
indicative  of  the  first  stage  in  the  opposite  apex. 

Mensuration. — If  a  cyrtometer  tracing  has  been  made  during  the  first 
stage  a  second  tracing  made  after  the  disease  has  advanced  to  the  second 
stage  shows  more  shrinkage  and  if,  in  the  meantime,  the  opposite  apex 
has  become  involved,  that  side  will  also  show  some  diminution  in  size. 

Auscultation. — The  breath  sounds  in  the  second  stage  of  the  disease 
are,  as  a  rule,  sharply  differentiated  from  those  heard  over  the  healthy 
lung  and  from  those  heard  in  the  first  or  incipient  stage.  The  granular, 
or  slightly  enfeebled  or  doubtful  broncho-vesicular  breathing  becomes 
definitely  broncho-vesicular;  the  latter  maybe  slightly  suppressed  or  may 
closely  approach  true  bronchial  breathing.  Bronchial  breathing  such 
as  is  heard  in  croupous  pneumonia,  when  the  lung  is  completely  solidified, 
is  not  common  in  tuberculosis.  This  is  because  the  infiltration  rarely 
becomes  massive,  as  a  rule  remnants  of  healthy  tissue  remain  between  the 
caseous  areas  and  thus  impart  a  vesicular  quality  to  the  respiratory 
murmur.  The  broncho-vesicular  breathing  may  therefore  be  slightly 
bronchial  in  character  or  very  markedly  so,  depending  on  the  density  of 
the  infiltration.  When  the  infiltration  has  destroyed  most  of  the  pul- 
monary tissue  in  a  given  area,  the  chief  characteristic  of  the  breath  sounds 
is  that  they  are  greatly  suppressed.  At  times  they  may  be  almost 
inaudible,  especially  if  rales  are  present. 

While  in  a  few  cases  broncho-vesicular  breathing  may  gradually  pass 
into  the  pure  bronchial  type  it  far  more  frequently  happens  that  caver- 
nous or  amphoric  breathing  appears  as  the  result  of  cavity  formation. 
At  the  lower  border  of  the  infiltrated  area,  cog-wheel  breathing  is 
frequently  heard. 

Vocal  resonance  is  a  sign  of  relatively  little  value.  It  is  usually  ex- 
aggerated and  the  increase  corresponds  closely  to  the  percussion  changes. 

Rales. — As  there  is  usually  an  associated  bronchitis  and  some  soften- 
ing of  the  caseous  areas  medium-sized  rales  are  common.  They  may  be 
very  numerous  or  one  may  hear  only  a  few  isolated  rales ;  the  latter  may 
be  constantly  present  or  may  be  heard  only  during  every  second  or 
third  inspiration  or  expiration.  Very  often  when  but  one  rale  is  heard 
it  has  a  peculiar  sticky  quality;  it  is  often  referred  to  as  a  mucous  click. 
By  some  it  is  considered  almost  pathognomonic  of  tuberculous  infiltra- 
tion. While  not  absolute,  one  is  safe  in  saying  that  the  more  numerous 
the  rales  the  greater  is  the  probability  of  softening  and  hence  the  more 
serious  the  outlook.     If  the  rales  have  a  metallic  quality,  a  cavity  may 


DISEASES    OF    THE    LUNGS  345 

be  suspected  even  if  other  signs  of  excavation  are  absent.  Some  crepi- 
tating rales  are  commonly  present  in  this  stage  but  in  some  instances 
they  are  not  heard  while  the  patient  is  breathing  naturally.  Having  the 
patient  cough  and  then  take  a  deep  breath,  however,  will  often  bring 
out  a  shower  of  fine  rales;  sometimes  deep  breathing  will  accomplish 
the  same  result. 

Accordingly  as  the  rales  diminish  or  increase  or  change  in  character 
one  is  often  able  to  foretell  the  probable  outcome  of  the  disease.  If  the 
rales  diminish  it  is  an  indication  that  the  associated  bronchitis  is  dis- 
appearing and  that  the  softening  of  the  caseous  areas  is  ceasing.  On 
the  other  hand,  if  the  rales  gradually  become  more  numerous  breaking 
down  of  the  lung  tissue  is  probably  taking  place. 

With  arrest  of  the  disease  the  rales,  particularly  the  medium-sized 
ones,  may  entirely  disappear.  The  crepitating  rales,  on  the  other  hand, 
may  persist  for  years  even  when  the  patient  is  entirely  free  from 
symptoms. 

Pleuritic  friction  sounds  are  frequently  heard  during  this  stage.  The 
friction  rub  may  occur  on  the  affected  side  or  it  may  be  heard  on  the  op- 
posite side.  It  is  often  difficult  to  distinguish  between  crepitating  rales 
located  in  the  lung  and  fine  pleural  crepitations.  At  times  these  fine 
crepitations  may  be  heard  over  both  the  upper  and  the  lower  portion  of 
one  lung.  While  it  is  not  always  possible  from  the  character  of  the  sound 
alone,  to  differentiate  them,  one  can  usually  judge  whether  the  rales  are 
entirely  due  to  infiltration  of  the  pulmonary  tissue  or  whether  those 
heard  over  the  lower  portion  of  the  lung  are  due  to  pleurisy,  by  the  char- 
acter of  the  symptoms.  If  the  entire  lung  is  infiltrated  the  patient  is 
almost  certain  to  have  serious  symptoms;  on  the  other  hand,  if  the  symp- 
toms are  mild  and  the  patient  in  good  condition  the  lower  portion  of  the 
lung  is  presumably  free  from  disease  and  the  rales  are  pleuritic. 

The  Heart. — In  many  instances  the  heart  presents  no  abnormalities. 
On  the  other  hand,  there  may  be  noted  in  this  stage  an  increase  in  the 
number  of  heart  beats  per  minute.  A  cardio-respiratory  murmur  is 
quite  frequently  encountered. 

The  nearer  the  disease  approaches  the  third  or  advanced  stage  the 
more  frequently  does  one  hear  abnormal  heart  sounds.  The  first  sound 
may  be  reduplicated  and  reduplication  and  accentuation  of  the  second 
pulmonic  sound  are  commonly  heard.  Accidental  murmurs  may  also  be 
heard  particularly  at  the  pulmonic  area.  As  a  rule  the  systolic  blood- 
pressure  is  low. 

Physical  Signs  in  the  Third  or  Advanced  Stage. — In  taking  up  a  con- 
sideration of  the  physical  signs  encountered  in  the  advanced  stage  of 
pulmonary  tuberculosis  the  task  is  at  once  very  easy  and  at  the  same 
time  very  difficult.  It  is  easy  because  inspection  alone  will  frequently 
indicate  that  serious  mischief  has  been  wrought  by  the  disease;  it  is  often 
difficult,  however,  to  indicate  the  exact  nature  of  the  damage  because  of 
the  extremely  varied  pathological  changes  which  are  present.  In  one 
and  the  same  lung  there  may  be  cavity  formation,  consolidation  and 
varying  degrees  of  infiltration;  and  in  addition  there  may  be  present  an 
effusion,  a  partial  pneumothorax,  or  involvement  of  the  pleura,  which 
further  complicates  the  picture. 

With  reasonable  care  in  the  examination  of  the  chest  the  examiner 
should  be  able  to  determine  the  approximate  amount  of  damage  present. 


346      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,  AND   DIAPHRAGM 

The  more  experienced  the  physical  diagnostician  the  more  clearly  will 
the  physical  signs  he  elicits  correspond  to  the  actual  pathological  changes. 

Inspection. — When  the  disease  has  progressed  to  this  stage  the  vast 
majority  of  individuals  present  the  appearance  so  familiar  to  all.  The 
most  dominant  feature  of  the  picture  is  the  extreme  emaciation,  a  fact 
that  gave  the  disease  its  first  name,  phthisis  or  the  wasting  disease.  The 
hair  presents  a  lanky,  lusterless  appearance,  the  temples  and  cheeks  are 
sunken  and  the  eyes  look  unnaturally  bright  and  feverish.  The  so-called 
hectic  flush  is  usually  present  and  is  more  marked  on  the  side  most  dis- 
eased; the  bright  color  of  the  cheeks  is  in  marked  contrast  to  the  blanched, 
waxy  appearance  of  the  surrounding  skin.  Flushing  of  the  cheeks  usu- 
ally occurs  synchronously  with  the  afternoon  rise  in  the  temperature 
but  may  be  noted  before  the  thermometer  shows  the  presence  of  fever. 

The  skin  is  usually  dry  and  very  often  scaly.  Pityriasis  versicolor 
is  frequently  noted,  especially  among  those  who  are  not  cleanly  in  their 
habits. 

Inspection  of  the  mouth  at  this  time  may  show  a  tuberculous  ulcera- 
tion of  the  tongue,  the  buccal  surface  of  the  cheeks,  the  tonsils  or  the 
pharynx. 

The  hands  in  many  cases  are  noticeably  altered.  In  the  vast  majority 
of  advanced  cases  the  finger  nails  present  a  slightly  bluish  color.  The 
nails  themselves  are  often  curved,  usually  from  side  to  side  but  they  may 
also  curve  over  the  end  of  the  finger.  Clubbing  of  the  fingers  is  not  so 
frequently  encountered  in  tuberculosis  as  usually  is  taught  and  when 
present  is  rarely  of  the  extreme  grade  seen  in  bronchiectasis,  congenital 
heart  disease,  or  empyema.  Clubbing  of  the  fingers  .and  extreme  curv- 
ing of  the  nails,  when  at  all  marked  in  pulmonary  tuberculosis,  are  usually 
evidences  that  the  disease  has  been  of  long  standing  and  that  there  is 
considerable  fibrosis  and  bronchial  dilatation  present  in  the  lungs. 
Clubbing  of  the  fingers  was  noted  at  the  Phipps  Institute  in  21.7  per 
cent.,  and  curving  of  the  nails  in  38.9  per  cent,  of  3551  cases. 

In  the  terminal  stages  of  the  disease  edema  of  the  lower  extremities 
is  not  infrequent.  A  small  percentage  of  cases  towards  the  end  show  a 
purpuric  eruption  usually  over  the  legs  and  thighs. 

Inasmuch  as  individuals  with  any  type  of  chest  may  acquire  the  dis- 
ease the  only  striking  features  in  many  instances  are  the  emaciation,  the 
sunken  interspaces  and  evidences  of  retraction  on  one  side  or  the  other. 

Inspection  will  usually  show  marked  flattening  at  both  apices  and 
retraction  and  lack  of  motion  at  one  base.  As  a  rule  the  motion  is  good 
at  the  base  of  the  lung  least  diseased. 

The  Heart. — More  or  less  displacement  of  the  heart  is  extremely  com- 
mon, being  present  in  about  two-thirds  of  advanced  cases.  This  often 
can  be  detected  by  inspection  but  in  many  instances  the  position  of  the 
heart  can  be  determined  only  after  percussion  and  auscultation,  or  an 
X-ray  examination. 

The  displacement  is  always  toward  the  affected  side  or  the  side  most 
diseased  and  is  caused  to  some  extent  by  traction.  In  some  instances  a 
contributing  factor  in  the  displacement  is  a  vicariously  hypertrophied 
lung  which  tends  to  crowd  the  heart  toward  the  affected  side.  Dis- 
placement toward  the  left  is  far  more  common  than  toward  the  right 
side  except  in  the  far-advanced  cases  when  the  two  sides  are  about  equally 
involved.     As  a  rule  the  displacement  to  the  left  is  more  pronounced 


DISEASES    OF    THE    LUNGS  347 

than  toward  the  right  partly  because  of  the  anatomical  position  of  the 
heart  and  partly  because  of  the  attachment  of  the  mediastinum  to  the 
central  tendon  of  the  diaphragm.  When  the  heart  is  drawn  toward  the 
left  it  is  also  apt  to  be  pulled  upward  toward  the  axilla. 

At  times  the  right-sided  displacement  may  be  so  marked  as  to  consti- 
tute a  dextro-cardia.  It  is  to  be  borne  in  mind  that  when  the  impulse 
is  noted  on  the  right  side  in  acquired  dextro-cardia,  it  is  caused  by  the 
right  ventricle. 

While  some  displacement  of  the  heart  unquestionably  takes  place, 
it  is  more  apparent  than  real.  This  is  due  to  the  retraction  of  the  chest 
wall  and  the  consequent  diminution  of  the  capacity  of  the  thorax  which 
naturally  alters  the  landmarks  with  reference  to  the  apex  beat. 

When  the  left  lung  is  extensively  diseased  and  retraction  takes  place 
there  is  often  a  marked  pulsation  in  the  second  and  third  interspaces  on 
the  left.  This  is  caused  by  the  exposure  of  the  right  auricle  which  in 
health  is  covered  by  pulmonary  tissue. 

Palpation  serves  to  confirm  the  lack  of  expansion  noted  on  inspection 
and  it  may  also  serve  to  locate  the  apex  beat. 

The  tactile  fremitus  will  vary:  at  the  apex  over  a  cavity  it  may  be 
increased  or  diminished.  In  other  portions  of  the  chest  it  will  be  in- 
creased or  not  according  to  the  amount  of  underlying  infiltration.  A 
rhonchal  fremitus  may  be  felt  at  times. 

Percussion.- — Assuming  that  there  is  a  cavity  the  size  of  an  orange 
in  the  upper  part  of  the  upper  lobe  with  dense  infiltration  below  it  which 
gradually  thins  out  as  the  base  of  the  lower  lobe  is  reached,  the  following 
percussion  changes  will  be  present :  Over  the  cavity  the  note  will  be  tym- 
panitic. It  is  low-pitched  and  may  have  an  amphoric  or  cracked-pot 
quality.  The  amphoric  note  is  similar  to  that  produced  by  percussing 
the  cheek  with  the  mouth  open;  the  cracked-pot  sound  can  be  reproduced 
by  striking  the  clasped  and  concave  hands  on  the  knee. 

Wintrich's  and  Gerhardt's  changes  of  note  are  always  referred  to  as 
aids  in  recognizing  a  cavity.  The  information  furnished  by  these  signs 
is  uncertain  and  of  little  value  when  present.  Personally  I  cannot  recall 
having  looked  for  them  for  years. 

Below  the  cavity  over  the  dense  infiltration  the  note  is  dull  or  nearly 
so;  as  the  base  is  approached  the  note  becomes  more  and  more  resonant. 
If  the  tubercles  are  widely  separated  in  the  inferior  portion  of  the  lung 
the  percussion  note  may  show  no  abnormality. 

Over  the  opposite  lung  the  disease  is  apt  to  be  less  extensive  and  the 
percussion  changes  correspondingly  less  marked.  A  cavity  may  be  pres- 
ent in  the  upper  lobe;  if  so  the  signs  given  above  may  be  elicited.  Other- 
wise, the  note  will  be  dull  and  gradually  shade  off  to  normal  as  the  base 
is  reached.  A  hyperresonant  note  may  be  present  over  the  base  of  the 
least  diseased  lung  as  the  result  of  compensating  emphysema. 

Percussion  of  the  lower  limits  of  the  lung  posteriorly  will  show  the 
side  most  affected  to  be  at  a  higher  level. 

Absolute  dulness  over  the  base  of  the  chest  in  an  advanced  case  of 
tuberculosis  may  or  may  not  mean  the  presence  of  fluid.  Not  un- 
commonly when  fluid  is  actually  present,  especially  if  purulent,  a  diagnosis 
of  advanced  tuberculosis  is  made.  If  the  dulness  is  due  to  tuberculosis 
there  will  be  rales  and  the  voice  sounds,  if  not  exaggerated,  williack  the 
distant  quality  so  commonly  present  when  fluid  exists. 


348       DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND   DIAPHRAGM 

Displacement  of  the  heart  may  be  shown  by  the  position  of  the  right 
and  left  borders  of  cardiac  dulness.  If  both  upper  lobes  are  extensively 
diseased,  however,  this  may  not  be  possible. 

Auscultation. — The  most  distinctive  feature  of  the  third  stage  of 
tuberculosis  is  the  presence  of  a  cavity  or  cavities.  While  a  cavity  may 
or  may  not  be  present  in  the  second  it  is  rarely  absent  in  the  third  stage 
although  it  may  not  be  possible  to  elicit  signs  which  will  indicate  its 
presence. 

Inasmuch  as  cavitation  is  so  universally  present  in  advanced  tuber- 
culosis of  the  lungs  a  somewhat  detailed  description  is  necessary.  It 
has  already  been  shown  in  the  section  dealing  with  the  morbid  anatomy 
of  the  disease  that  a  tuberculous  cavity  is  usually  located  in  the  upper 
lobes,  at,  or  near,  the  apex.  In  an  analysis  made  by  Ewart  cavitation 
occurred  at: 

The  apices 282  times. 

Dorso-axillary  region 227  times. 

Mammary  region 189  times. 

Sternal  region 61  times. 

Base ".  32  times. 

In  50  consecutive  cases  which  I  studied  at  the  Phipps  Institute  there 
were  in  all  76  cavities  present,  the  distribution  being  as  follows: 

Right  upper  lobe 15 

Left  upper  lobe 6 

Both  upper  lobes 30 

Middle  lobe  (right  side) 1 

Left  lower  and  both  upper  lobes 1 

The  location  of  the  cavity  with  reference  to  the  chest  wall  has  more 
to  do  with  its  recognition  than  the  size  of  the  excavation.  A  small 
cavity,  no  larger  than  a  cherry,  may  give  signs  if  situated  just  beneath 
the  pleura.  If,  on  the  other  hand,  the  cavity  is  deeply  seated  it  may  be 
the  size  of  a  small  orange  and  still  give  no  signs.  This  is  especially 
the  case  with  cavities  situated  in  the  center  of  the  lower  lobes  (Figs. 
260,  261,  262). 

While  in  most  instances  the  approximate  size  of  the  cavity  can  be 
determined  by  physical  signs  this  is  not  always  possible.  A  small 
cavity  surrounded  by  densely  infiltrated  tissue  will  often  give  the  impres- 
sion that  there  is  a  very  large  excavation.  It  is  not  possible  to  determine 
with  anj^  degree  of  certainty  as  to  whether  the  excavation  is  single  or 
consists  of  a  number  of  communicating  cavities.  If  gurgling  and 
resonating  rales  are  heard  over  a  wide  area  a  honeycombed  condition 
of  the  lung  is  to  be  suspected;  especially  if  the  disease  is  of  the  acute 
broncho-pneumonic  type  in  which  breaking  down  of  the  lung  tissue  is 
rapid. 

The  character  of  the  breath  sounds  heard  over  a  cavity  is  in  the 
majority  of  instances  cavernous  or  amphoric  in  quality  and  maybe  loud 
and  distinct  or  very  distant.  In  some  instances  the  breath  sounds  are 
bronchial  in  quality  probably  owing  to  consolidation  about  the  cavity. 
It  is  to  be  noted  that  in  spite  of  other  well-marked  signs  of  excavation 
the  breath  sounds  may  be  almost  inaudible;  in  very  large  cavities  abso- 
lute silence  over  the  upper  part  is  not  unusual. 


DISEASES    OF    THE    LUNGS  349 

Exaggeration  of  both  the  spoken  and  whispered  voice  sounds  is  the 
rule.  Whispering  pectoriloquy  while  not  pathognomonic  of  cavita- 
tion is  the  sign  most  constantly  present.  Laennec  in  speaking  of  pec- 
toriloquy (and  the  same  applies  to  whispering  pectoriloquy)  states  that 
the  intensity  and  perfection  of  this  phenomenon  ranges  from  that  which 
is  unmistakable  to  that  which  is  of  doubtful  import.  "The  circum- 
stances that  concur  to  render  pectoriloquy  perfect  are:  complete  empti- 
ness of  the  excavation,  increased  density  of  the  pulmonary  tissue  forming 


Fig.  260. — A  chronic  type  of  disease.  Anteriorly  just  behind  the  clavicle  is  a  large 
walled-off  cavity  which  has  been  formed  by  the  coalescence  of  several  small  ones.  Remain- 
der of  right  upper  lobe  and  the  anterior  portion  of  lower  lobe  contains  much  fibrous  tissue. 

its  walls,  its  easy  communication  with  one  or  more  bronchial  tubes  of 
some  magnitude,  and  its  proximity  to  the  parietes  of  the  chest." 

The  sound  produced  by  coughing  very  often  has  a  metallic  or  amphoric 
quality  and  when  present  is  very  suggestive  of  excavation. 

Rales  may  or  may  not  be  heard  over  the  excavation.  In  chronic 
quiescent  cases  the  cavity  may  be  dry  and  no  rales  will  be  heard.  In 
active  cases  rales  are  almost  always  heard  and  are  often  metallic  or 
resonating  in  quality.  In  my  experience  the  presence  of  rales  having  a 
metallic  quality  is  the  most  certain  sign  we  possess. 

In  a  clinical  and  post-mortem  study  of  cavities  I  found  that  in  50 


350      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

cases  there  were  present  76,  of  which  58  were  recognized  during  life.  The 
18  escaping  detection  were,  for  the  most  part,  small  and  centrally  located. 
Basing  the  value  of  the  various  signs  on  the  frequency  with  which  each 
occurred,  the  following  results  were  obtained: 

Per 
Cent. 

Whispering  pectoriloquy 53  out  of  58  (91.3) 

Tympany  (on  percussion) 39  out  of  58  (67.4) 

Cavernous  or  amphoric  breathing 38  out  of  58  (65.5) 

Gurgling  or  consonating  rales 33  out  of  58  (58.6) 


Fig.  261. — Cavity  in  right   upper  lobe   posteriorly.     Physical   signs   elicited  posteriorly 
only.     Rest  of  right  upper  lobe  air-bearing  but  contains  a  good  deal  of  fibrous  tissue. 

Although  none  of  the  above  signs  are  pathognomic  of  a  cavity  the 
presence  of  any  one  of  them  is  suggestive  and  the  probability  of  its  exist- 
ence is  increased  by  combinations  of  any  two  or  more  of  them.  Two 
sources  of  error  are  to  be  borne  in  mind:  (1)  Consolidated  pulmonary 
tissue  about  a  bronchus  may  give  rise  to  the  same  phenomena.  This 
mistake  was  made  in  five  instances  in  the  series  I  studied.  (2)  The  origin 
of  a  single  cavity  at  the  right  or  left  apex  may  be  transmitted  across  the 


DISEASES    OF   THE    LUNGS  351 

spine  and  lead  to  a  diagnosis  of  a  cavity  at  both  apices.  This  error 
can  be  avoided  by  tracing  the  sounds  from  their  origin  when  they  will 
be  found  to  diminish  in  intensity  the  farther  the  bell  of  the  stethoscope 
is  moved  from  the  site  of  the  cavity. 

The  auscultatory  signs  over  the  remainder  of  the  chest  parallel 
those  of  percussion.  Below  the  cavity  the  infiltration  is  apt  to  be  dense 
and  the  breath  sounds  bronchial  or  broncho-vesicular  in  character.  The 
latter  type  of  breathing  is  usually  present  over  the  base  of  the  side  most 


Fig.  262. — Two  small  cavities  situated  at  some  distance  from  the  posterior  pleura.     Deeply 
seated  cavities  are  apt  to  escape  detection  by  physical  signs. 

affected  and,  in  addition,  may  be  more  or  less  suppressed.  The  voice 
sounds  are  more  or  less  exaggerated  depending  on  the  density  of  the 
infiltration. 

Over  the  opposite  lung  there  may  be  signs  of  a  cavity  at  the  apex  and 
evidences  of  infiltration  beneath  it  but  rarely  as  well  marked  as  on  the 
side  most  diseased.  Over  the  lower  lobe  the  breath  sounds  are  usually 
puerile  in  type  due  to  compensatory  emphysema.  Although  at  the  au-- 
topsy  table  scattered  tubercles  are  usually  found  in  the  emphysematous 
lower  lobe  they  give  no  evidence  of  their  presence  during  life.  They 
probably  represent,  for  the  most  part,  a  terminal  infection  such  as  occurs 
in  the  other  viscera. 


352      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

In  the  advanced  stage  tachycardia  is  the  rule,  and  the  muscle  tone  of 
the  first  sound  is  poor.  Accentuation  and  reduplication  of  the  second 
pulmonic  sound  is  common;  less  frequently  these  changes  are  noted  in 
the  first  sound.  Functional  murmurs  are  frequent  and  are  generally 
heard  at  the  pulmonic  area.  Irregularity  of  the  cardiac  rhythm  is  noted 
in  a  few  instances. 

Diagnosis. — The  recognition  of  pulmonary  tuberculosis  in  its  different 
stages  must  take  into  account  four  factors : 

1.  A  clear  conception  of  the  morbid  anatomy  of  the  disease;  the  loca- 
tion of  the  primary  lesion;  how  it  first  manifests  itself;  the  "line  of  march" 
as  it  progresses;  and  finally  the  character  of  the  lesions  it  produces. 

2.  There  must  be  a  proper  appreciation  of  the  significance  of  the 
symptoms  and  sufficient  moral  courage  to  act  promptly  even  when  the 
appearance  of  general  good  health  seems  to  deny  the  presence  of  serious 
trouble.  It  should  never  be  forgotten  that  the  onset  is  usually  insidious 
and  the  early  manifestations  indefinite.  To  delay  the  diagnosis  until  the 
evidence  is  unequivocal  is,  only  too  often,  to  let  slip  the  opportunity  most 
favorable  to  restore  health. 

3.  It  cannot  be  too  strongly  emphasized  that  the  diagnosis  of  pul- 
monary tuberculosis,  particularly  in  the  first  stage,  is  not  to  be  based 
exclusively  on  the  presence  or  absence  of  physical  signs.  "Invaluable 
as  they  are,  their  importance  is  greatly  enhanced  by  association  with 
symptoms  and  the  knowledge  of  pathological  laws.  Not  only  are  we 
to  avoid  exclusive  reliance  on  the  presence  or  absence  of  physical  signs, 
but  it  is  also  to  be  borne  in  mind  that  physical  signs,  while  often  indicat- 
ing the  extent  and  degree  of  pulmonary  damage,  convey  no  direct  infor- 
mation as  to  the  pathological  nature  of  those  changes." 

4.  It  is  necessary  to  employ  in  every  case  one  or  all  of  the  avail- 
able laboratory  aids.  There  can  be  ho  excuse  for  neglecting  the  examina- 
tion of  the  sputum.  In  many  instances  this  may  seem  superfluous.  It 
is  to  be  borne  in  mind,  however,  that  there  are  many  conditions  which 
simulate  both  the  symptoms  and  physical  signs  of  tuberculosis  and  are 
only  to  be  distinguished  from  it  by  examination  of  the  sputum. 

The  significance  of  the  tuberculin  tests  will  be  discussed  later. 
The  advantages  and  disadvantages  of  the  Roentgen  rays  are  also  con- 
sidered elsewhere.  The  complement  fixation  test  is  still  too  recent  to 
properly  estimate  its  usefulness. 

Diagnosis  of  Healed  and  Arrested  Lesions. — Very  frequently  one 
encounters  individuals  with  abnormal  signs  at  one  or  the  other  apex.  In 
such  a  case  the  question  will  arise:  Is  this  an  incipient  lesion  or  is  it  the 
result  of  trouble  which  has  occurred  in  the  past  and  has  undergone 
spontaneous  cure? 

The  physical  signs  are  not  conclusive.  The  clavicle  may  be  unduly 
prominent  and  slight  flattening  with  restriction  of  expansion  may  be 
noted  beneath  the  clavicle,  indicating  some  shrinkage  at  the  apex.  The 
breath  sounds  may  be  slightly  suppressed  or  broncho-vesicular  in  type. 
The  voice  sounds  are,  as  a  rule,  exaggerated.     There  are  no  rales. 

These  signs  differ  in  no  respect  from  those  found  in  the  early,  active 
stage  of  the  disease.  In  such  cases  the  question  as  to  whether  the  lesion 
is  active,  or  healed  and  quiescent,  will  rest  on  the  presence  or  absence  of 
symptoms.  If  there  is  no  cough  or  expectoration,  no  fever,  no  loss  of 
weight  and  there  has  been  no  evidence  of  blood  in  the  sputum  or   an 


DISEASES    OF   THE    LUNGS  353 

attack  of  pleurisy  within  the  past  year  or  two,  one  may  assume,  with 
reasonable  certainty,  that  the  signs  are  indicative  of  an  old  tuberculous 
infection  which  during  its  active  stage  was  so  mild  as  to  escape  notice. 
Occasionally  signs,  such  as  those  mentioned  above,  may  be  caused  by  non- 
tuberculous  infections. 

The  subcutaneous  injection  of  tuberculin  has  been  advised  to  dis- 
tinguish between  a  healed  and  an  early  active  lesion.  If  healed  there 
may  be  slight  constitutional  reaction  (fever,  malaise,  joint  pains)  but  no 
focal  reaction ;  the  latter  consists  of  rales  over  the  suspected  area  and  the 
development  of  a  slight  cough  with  possibly  some  expectoration  in  addi- 
tion to  the  constitutional  symptoms.  The  use  of  tuberculin  as  a  diag- 
nostic agent  will  be  considered  in  another  place. 

Another  type  of  case  is  that  in  which  there  are  evidences  of  extensive 
pulmonary  damage  and  in  which  the  patient  has  some  cough  and  expecto- 
ration but  no  constitutional  symptoms.  Such  a  case  may  or  may  not 
have  been  under  treatment  when  first  seen.  If  one  judges  by  the  phys- 
ical signs  alone  the  patient  may  be  considered  to  be  in  a  serious  condi- 
tion and  may  be  advised  to  abandon  his  business  and  enter  a  sanatorium 
at  once.  The  course  to  be  pursued  will  depend  entirely  on  the  general 
condition  of  the  patient's  health  and  the  presence  or  absence  of  symp- 
toms denoting  activity  of  the  disease. 

A  woman  whom  I  have  had  under  observation  for  ten  years  has  at  the 
present  time  the  same  physical  signs  as  when  originally  seen,  namely,  signs 
of  a  cavity  at  each  apex  and  impairment  of  the  percussion  note,  feeble 
broncho-vesicular  breathing  and  fine  rales  extending  down  to  the  fourth 
rib  on  the  right  side.  Her  general  health  is  excellent,  although  she  has 
an  occasional  hemoptysis,  and  she  lives  the  life  of  a  normal  individual. 
Twice  within  the  past  two  years,  because  of  an  attack  of  blood  spitting, 
she  has  consulted  men  of  large  experience  in  tuberculosis  work.  In  both 
instances  she  was  given  an  unfavorable  prognosis  and  advised  to  enter  a 
sanatorium  at  once.  Cases  such  as  this  one  are  not  infrequently  seen  and 
illustrate  very  clearly  that  entire  dependence  cannot  be  placed  upon  the 
physical  findings  alone.  One  of  the. peculiar  features  of  tuberculosis  is 
that  very  often  with  the  existence  of  extensive  pulmonary  damage  the 
symptoms  are  negligible  and  the  patient  enjoys  fairly  good  health;  on 
the  other  hand,  physical  signs  may  be  very  slight  or  even  absent,  and  the 
symptoms  will  be  of  the  most  serious  nature. 

Examination  of  the  Sputum. — The  examination  of  the  sputum  for 
tubercle  bacilli  is  a  very  simple  procedure,  the  details  of  which  are 
familiar  to  every  one.  While  the  presence  of  tubercle  bacilli  in  the 
sputum  is  absolute  proof  that  a  pulmonary  tuberculosis  exists,  their 
absence  is  no  assurance  that  the  patient  is  free  from  the  disease.  In 
the  earliest  stage  of  tuberculosis  the  sputum  will  be  found  negative  for 
tubercle  bacilli  in  from  60  to  75  per  cent,  of  cases  It  is  most  important 
that  this  fact  should  be  known.  Many  practitioners  fail  to  realize 
this  and  are  satisfying  both  themselves  and  the  patient  that  tuberculosis 
is  not  present  as  the  result  of  one  or  two  negative  examinations.  I 
repeat,  therefore,  that  in  the  early  stage  of  the  disease,  one,  or  even  half 
a  dozen,  negative  examinations  mean  nothing. 

Another  very  common  error  is  that  of  assuming  the  case  to  be  one  of 
advanced  pulmonary  tuberculosis  because  the  symptoms  -_and  physical 
signs  seem  to  clearly  indicate  it  as  such.     Inasmuch  as  the  diagnosis 

23 


354      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

seems  certain  the  sputum  is  not  examined.  It  is  because  of  this  neglect 
that  many  cases  of  bronchiectasis,  pneumoconiosis,  chronic  empyema,  the 
mycotic  infections  and  even  chronic  carclio-renal  disease,  are  mistaken 
for  tuberculosis.  A  single  negative  examination  in  a  case  with  extensive 
pulmonary  damage  demands  that  the  examination  be  repeated  until 
tubercle  bacilli  are  actually  found  or  until  a  sufficient  number  of  nega- 
tive examinations  make  it  clear  that  some  process  other  than  tuberculosis 
is  present.  While  in  the  majority  of  instances  the  presence  or  absence  of 
tubercle  bacilli  is  all  that  need  be  determined,  one  should  always  be  alive 
to  the  possibility  of  other  sources  of  infection. 

The  conditions  which  simulate  tuberculosis  and  which  are  recogniz- 
able by  the  examination  of  the  sputum,  although  not  numerous,  should 
always  be  kept  in  mind  if  tubercle  bacilli  cannot  be  found.  In  default 
of  any  demonstrable  organism,  such  as  the  tubercle  bacillus,  actinomyces, 
blastomyces,  aspergillus,  ova  of  the  lung  fluke,  etc.,  the  pulmonary 
trouble  may  be  due  to  malignant  disease,  syphilis,  or  some  chronic  in- 
flammatory condition  such  as  cirrhosis  of  the  lung  or  pneumoconosis. 
If  one  is  not  familiar  with  the  bacteriological  characteristics  of  the  rarer 
forms  of  infection  the  sputum  should  be  sent  to  a  competent  bacteriolo- 
gist for  examination. 

Of  the  various  infecting  agents  which  produce  lesions  similar  to 
tuberculosis  there  is  only  one  that  bears  any  resemblance  to  the  tubercle 
bacillus,  namely,  certain  forms  of  the  streptothrix  group.  To  those  who 
are  not  thoroughly  familiar  with  the  morphology  of  the  tubercle  bacillus 
small  acid-fast  rods  may  be  mistaken  for  Koch's  bacillus.  The  strep- 
tothrix may  occur  as  an  independent  organism  but  is  more  often  en- 
countered as  part  of  the  mixed  infection  in  cases  of  tuberculosis  with 
cavity  formation  and  in  cases  of  bronchiectasis.  It  is  to  be  borne  in 
mind  that  the  bacillus-like  rods  of  the  streptothrix  occur  in  chains  in- 
stead of  being  clumped  and  that  they  are  decolorized  with  30  per  cent, 
nitric  acid.  They  are  often  resistant  to  20  per  cent,  sulphuric  acid  and 
Gabbet's  stain. 

At  one  time  it  was  believed  that  the  number  of  tubercle  bacilli  pres- 
ent in  the  entire  slide  or  if  numerous,  the  average  number  per  field,  was 
of  value  in  determining  the  probable  outcome  of  the  disease.  It  is 
now  recognized  that  the  number  of  bacilli  per  field  at  the  time  of  the 
first  examination  is  no  indication  of  either  the  severity  or  the  extent 
of  the  disease.  From  40  to  50  bacilli  to  each  field  may  be  present  in  an 
early,  mild  case;  on  the  other  hand,  the  bacilli  may  be  very  few  in 
number  in  a  case  which  begins  with  severe  symptoms  and  progresses 
steadily  to  a  fatal  termination.  In  a  general  way  a  gradual  diminution 
of  the  number  of  bacilli  at  each  successive  examination,  is  of  favorable 
import.  And  on  the  other  hand,  a  rapid  increase  in  the  number  is  apt 
to  be  an  indication  that  the  process  is  extending  and  the  lung  tissue  is 
breaking  down.  Much  more  reliable  indications  as  to  how  the  disease 
is  behaving  are  to  be  found  in  the  patient's  general  condition,  the  abate- 
ment of  symptoms  and  stationary  or  retrogressive  physical  signs. 

The  examination  of  the  sputum  for  tubercle  bacilli  is  so  simple  a 
procedure  that  the  statement  that  they  have  been  found  in  the  sputum 
is  usually  accepted  as  being  true.  In  common  with  other  methods  of 
diagnosis,  however,  the  reliability  of  a  sputum  examination  depends 
to  some  extent  on  the  experience  of  the  examiner.     Unless  my  own  ex- 


DISEASES    OF    THE    LUNGS  355 

perience  is  unique,  I  am  inclined  to  believe  that  many  positive  reports 
are  being  made  which  in  reality  are  negative.  Within  the  past  few  years 
I  have  seen  five  cases  in  which  tubercle  bacilli  were  said  to  be  present  in 
the  sputum.  In  one  case  the  autopsy  failed  to  show  any  evidence  of 
tuberculosis.  In  the  others  a  most  thorough  study  of  the  sputum,  in- 
cluding animal  inoculations,  failed  to  show  the  organism.  In  addition 
the  subsequent  history  of  the  patients  made  it  evident  that  a  mistake  had 
been  made.  If  there  is  any  doubt  as  to  the  reliability  of  the  examiner 
one  should  examine  the  sputum  oneself  or  send  it  to  a  reliable  laboratory. 

In  patients  in  whom  tuberculosis  is  suspected  but  who  have  no  spu- 
tum, the  administration  of  iodide  of  'potassium  has  been  recommended. 
This  procedure  cannot  be  condemned  too  strongly.  As  it  is  now  quite 
generally  recognized  that  iodide  of  potassium  is  very  apt  to  cause  a  break- 
ing down  of  tuberculous  foci  in  the  lungs  there  is  little  to  be  said  in  favor 
of  using  the  drug  for  diagnostic  purposes.  By  so  doing  a  quiescent  lesion 
which  is  giving  no  trouble  may  be  aroused  into  activity. 

Tuberculin  Tests. — The  accepted  belief  at  the  present  time  is  that  a 
positive  reaction  to  one  of  the  tuberculin  tests  is  indicative  of  a  tuber- 
culous lesion  somewhere  within  the  body.  A  positive  test  does  not 
mean,  however,  that  the  individual  has  clinical  tuberculosis.  It  must  be 
clearly  kept  in  mind  that  there  is  a  great  difference  between  tuberculosis 
that  is  clinically  recognizable  and  hyper  sensitiveness  to  tuberculin. 
Hypersensitiveness  is  extremely  common,  and  is  encountered  in  a  large 
proportion  of  healthy  people,  the  frequency  with  which  it  is  met  increas- 
ing rapidly  from  the  second  year  of  life.  It  is  a  great  mistake  to  assume 
that  because  an  individual  reacts  to  some  one  of  the  tuberculin  tests  that 
he  is  tuberculous  in  the  sense  that  he  needs  active  treatment;  and,  as 
I  shall  later  point  out,  a  negative  tuberculin  test  does  not  entirely  free 
us  from  responsibility. 

In  regard  to  the  tests  themselves  there  are  certain  facts  which  should 
be  kept  in  mind.  First,  as  regards  the  subcutaneous  test.  At  one  time 
the  test  was  extensively  used  in  adults  and  a  positive  reaction  was,  and 
by  many  still  is,  regarded  as  conclusive  proof  that  the  individual  has 
tuberculosis.  Of  recent  years,  however,  some  observers  have  warned 
against  its  use,  pointing  out  that  the  test  is  capable,  in  certain  instances, 
of  stirring  an  inactive  lesion  into  an  active  one.  Furthermore,  there  is 
now  a  tendency  not  only  to  limit  the  use  of  the  test,  but  in  addition  to 
ignore  the  constitutional  symptoms  of  a  reaction  (such  as  fever,  joint 
pains,  local  reaction,  etc.)  and  to  call  positive  only  those  cases  which 
give  a  focal  reaction,  such  as  rales  at  a  suspected  apex,  or  some  pain, 
redness,  and  swelling  in  a  suspected  joint. 

The  cutaneous  or  von  Pirquet  test  has  achieved  enormous  popularity  by 
reason  of  its  simplicity,  and  also  because  it  is  widely  credited  with  being 
a  positive  indication  of  tuberculosis.  In  children  under  two  years  of 
age  it  furnishes  valuable  evidence  when  positive  and  usually  means 
clinical  tuberculosis.  Beyond  the  second  year,  however,  it  loses  much 
of  its  positive  value,  and  the  older  the  child  the  more  unreliable  it  is 
as  an  evidence  of  true  tuberculosis. 

The  precutaneous  or  so-called  Moro  test  has  about  the  same 
significance. 

Finally,  we  have  to  consider  the  conjunctival  test  introduced  by 
Wolff-Eisner  and  Calmette.     The  majority  of  observers  have  come  to 


356      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

regard  this  test  as  dangerous,  because  of  the  possibility  of  producing  an 
inflammatory  condition  which  may  lead  to  serious  damage  of  the  eye. 
According  to  Hamman  and  Wolman,1  who  have  employed  the  test  in  a 
large  series  of  cases,  the  test  is  free  from  danger,  and  is  superior  to  the 
Moro  and  von  Pirquet  tests  in  that  it  is  not  so  sensitive  and  that  a  posi- 
tive reaction  points  strongly  to  an  active  rather  than  a  latent  process, 
especially  so  when  supported  by  other  indications. 

The  question  naturally  arises :  What  is  the  practical  value  of  the  von 
Pirquet  or  Moro  test  in  determining  the  individuals  who  have  true 
tuberculosis  and  those  who  can  be  disregarded?  We  are  forced  to  con- 
clude that  they  are  of  little  value  except  as  an  evidence  of  hypersensi- 
tiveness.  In  a  series  of  children  studied  by  Kaufman  and  myself2  we 
repeatedly  saw  anemic,  under-nourished  children  with  or  without  tuber- 
culous parents  who  gave  no  reaction;  and,  on  the  other  hand,  we  en- 
countered children  who  presented  no  physical  signs;  who  were  in  robust 
health,  and  who  had  violent  skin  reactions. 

The  X-ray  in  the  Diagnosis  of  Pulmonary  Tuberculosis. — The  ques- 
tion of  the  relative  merits  of  the  X-rays  and  the  ordinary  method  of 
physical  examination  in  incipient  or  early  tuberculosis  is  still  sub  judice. 
Clinicians  are  not  in  agreement  as  to  the  superiority  of  the  newer  over  the 
older  method  and  between  the  clinicians  and  the  roentgenologists  there 
is  a  wide  breach.  The  latter,  with  few  exceptions,  arrogate  unto  them- 
selves an  ability  to  recognize  early  tuberculous  lesions  in  the  lungs  which 
is  not  warranted.  In  the  first  place  the  earliest  manifestations  of  tuber- 
culosis as  shown  on  the  roentgenogram,  are  not  distinctive.  Many 
simple  chronic  infections  will  give  the  same  picture.  Again,  as  Friedrich 
Miiller,  Holzknecht  and  others  have  pointed  out  a  deposit  of  a  few  early 
tubercles  with  accompanying  catarrh,  and  which  constitute  an  anatom- 
ically incipient  case,  will  not  cast  a  shadow  on  the  plate.  Active  dry 
pleurisy  also  gives  no  hint  of  its  presence  whatsoever,  so  far  as  the 
roentgenogram  is  concerned. 

Many  roentgenologists  claim  that  an  early  tuberculous  process  is 
distinctive  without  realizing  that  other  infectious  processes  of  the  lung, 
of  whatever  character,  generally  spread  along  the  course  of  the  air 
passages.  As  Baetjer3  has  pointed  out,  these  become  inflamed  and, 
as  in  all  inflammatory  conditions,  they  produce  reaction,  consequently 
the  fibrous  sheath  which  surrounds  the  bronchi,  artery,  vein  and  lymph 
channels  becomes  thickened.  It  is  just  this  type  of  cases  that  it  is  so 
important  to  make  an  etiological  diagnosis.  Although  the  clinical  evi- 
dence and  the  physical  signs  in  such  cases  may  be  inconclusive,  the 
roentgenogram  is  equally  so,  for  while  changes  may  be  shown  in  the  plate 
it  is  impossible  to  state  whether  they  are  due  to  tuberculosis  or  some  other 
infection.  It  is  only  when  the  tuberculous  lesion  has  become  sufficiently 
advanced  that  a  definite  opinion  can  be  given  as  to  its  nature.  When 
this  point  has  been  reached  an  appeal  to  the  roentgenogram  is  not  neces- 
sary as  all  the  signs  and  symptoms  of  the  disease  are  apparent  from  the 
clinical  side. 

Another  disputed  point  is  the  question  as  to  whether  it  is  possible  by 
roentgenography  to  determine  whether  a  tuberculous  lesion  is  active  or 

1  "Tuberculin  in  Diagnosis  and  Treatment,"  1912. 

2  Am.  Jour,  of  Med.  Sc,  October.  1914. 

3  International  Clinics,  Twenty-sixth  Series,  vol.  iii,  1916. 


DISEASES    OF    THE    LUNGS  357 

inactive.  Many  roentgenologists  claim  that  such  a  distinction  can  be 
made.  Baetjer  takes  the  stand  that  such  a  differentiation  cannot  be 
made,  and  in  this  opinion  I  concur.  The  activity  or  inactivity  of  a 
tuberculous  lesion  is  to  be  determined  by  symptoms  and  neither  physical 
signs  nor  radiography  can  determine  this  point. 

At  the  present  time  the  use  of  the  X-ray  is  too  recent  to  determine 
what  its  ultimate  status  will  be.  It  is  fair  to  assume,  however,  that  those 
who  now  oppose  it  will  eventually  take  a  more  liberal  view  and,  on  the 
other  hand,  it  is  equally  certain  that  roentgenologists  will  have  to  modify 
their  claims.  Already  there  are  signs  pointing  to  the  latter  view.  Not 
so  long  ago  tremendous  importance  was  attached  to  root  shadows.  Now 
we  hear  less  about  these  "visionary  interpretations,"  as  Osier  termed 
them.  The  elimination  of  root  shadows  has  been  brought  about  largely 
by  improved  technique,  chiefly  in  the  substitution  of  the  stereoscopic 
for  the  single  plate. 

What  is  needed  beyond  everything  else  to  establish  the  true  status 
of  the  X-rays  in  pulmonary  disease  is  the  anatomical  corroboration  of  such 
findings.  Anatomical  proof  was  the  foundation  upon  which  the  art  of 
physical  diagnosis  was  reared.  Until  this  proof  is  forthcoming  it  is 
inevitable  that  differences  of  opinion  will  occur.  Such  proof  can  be  fur- 
nished only  by  combining  the  observations  of  the  clinician,  the  radiog- 
rapher and  the  pathologist.  An  investigation  of  this  kind  "requires 
the  most  patient  following  up  of  cases,  it  may  be  over  long  periods,  in  the 
hope  that  even  one  single  case,  which  has  been  carefully  and  accurately 
investigated  clinically  and  radiographically,  will  reveal  itself  to  the 
pathologist"  (Barty  King). 

Although  the  value  of  the  X-ray  in  the  diagnosis  of  early  tuberculosis 
still  remains  to  be  proved,  there  can  be  no  question  as  to  its  advantages 
in  showing  the  extent  of  the  lesion  and  in  the  detection  of  encysted 
empyema  or  a  partial  pneumothorax.  Minor1  after  years  of  experience, 
has  found  the  fluoroscope  of  service  for  this  purpose.  By  its  use  the 
topographical  distribution  of  the  lesions  can  be  made  out  readily  and  in 
addition  collections  of  pus  or  other  obscure  conditions  can  be  detected. 
This  method  has  the  advantage  of  not  requiring  special  training  as  does 
the  making  of  the  stereoscopic  plates. 

CHRONIC   TUBERCULOSIS  IN  EARLY  LIFE 

Morbid  Anatomy. — It  must  be  borne  in  mind  that  the  clinical  forms  of 
human  tuberculosis  in  different  ages  possess  correspondingly  different 
anatomical  features,  a  knowledge  of  which  is  necessary  for  the  under- 
standing of  the  interpretation  of  physical  signs.  In  the  majority  of  in- 
stances, tuberculosis,  when  it  involves  the  lungs  of  infants  and  young 
children,  is  bilateral,  widespread  (either  of  the  miliary  or  broncho-pneu- 
monic form),  and  acute  in  character. 

In  the  adult,  on  the  other  hand,  the  disease  begins  at  one  or  the  other 
apex,  follows  a  fairly  definite  course  in  its  progress,  and  is  chronic  in 
character,  although  subject  to  periods  of  acute  activity.  As  a  rule  the 
clinical  manifestations  of  tuberculosis  as  they  occur  in  infants  and  young 
children  differ  from  the  adult  type,  and  this  is  not  altered  by  the  fact 
that  the  juvenile  type  may  occur  in  adults,  and  vice  versa. 

1  International  Clinics,  Twenty-sixth  Series,  vol.  ii,  1916. 


358      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND  DIAPHRAGM 

Symptoms. — The  symptomatology  of  tuberculosis  in  adults,  while 
subject  to  many  vagaries,  is  invaluable  in  making  a  diagnosis.  Indeed 
in  many  cases  of  incipient  tuberculosis  it  is  our  chief  reliance  in  determin- 
ing the  nature  of  the  trouble.  In  children,  on  the  other  hand,  we  are 
deprived  of  much  of  the  value  of  symptoms,  because  of  the  inability  of 
young  children  to  give  a  correct  description  of  their  trouble;  nor,  as  a 
rule,  can  the  parents  throw  much  light  on  the  question. 

One  of  the  most  reliable  means  of  detecting  early  tuberculosis  in  the 
adult  is  the  slight  rise  in  temperature  which  may  occur  daily  or  only 
every  few  days.  In  children,  however,  little  reliance  can  be  placed  in 
these  slight  elevations  of  temperature,  for  the  reason  that  growing  chil- 
dren normally  have  a  higher  temperature  than  adults.  Landois1  gives 
as  the  normal  limits  99.5°  to  100.1°F.  (37.87°  to  37.62°C.)  in  children  from 
five  to  nine  years.  The  reason  for  this  is,  in  all  probability,  a  more 
active  metabolism,  although  other  influences  of  undetermined  origin 
may  also,  in  part,  be  contributory. 

Physical  Signs. — In  taking  up  the  question  of  physical  signs  in  the 
chest  of  infants  and  young  children  we  have  to  consider  what  is  probably 
the  most  difficult  phase  in  the  art  of  physical  diagnosis.  And  while  it 
is  true  that  the  underlying  principles  which  enable  us  to  detect  disease 
in  the  chest  are  the  same,  whether  it  be  adult  or  child,  there  are  certain 
differences  between  the  two  which  must  be  kept  in  mind.  Generally 
speaking  the  man  whose  training  has  been  confined  to  the  examination  of 
adults  alone,  or  children  alone,  is  likely  to  draw  false  conclusions  when  he 
invades  one  or  the  other  field,  and  much  that  has  been  written  regard- 
ing the  presence  of  chronic  tuberculous  lesions  in  the  lungs  of  children 
has  been  contributed  by  those  whose  standards  have  been  obtained  by 
the  examination  of  adults  with  tuberculosis. 

It  is  not  altogether  easy  to  fix  definitely  the  age  period  at  which  the 
signs  peculiar  to  children  cease.  Some  have  arbitrarily  fixed  this  limit 
at  the  age  of  six  years,  although  from  my  own  experience  ten  years  would 
be  more  nearly  correct. 

Probably  the  most  distinctive  difference  between  the  adult  and  the 
child  is.  that  in  the  latter  all  of  the  sounds  are  exaggerated.  Not  only  is 
the  breathing  of  the  familiar  puerile  type,  but  all  the  vocal  sounds  are 
increased,  and  in  addition  the  percussion  note  is  commonly  hyperresonant. 

As  an  illustration  of  how  the  exaggeration  of  physiologically  normal 
signs  may  be  misinterpreted  in  the  child  it  is  interesting  to  note  that 
79  children,  out  of  362  studied  at  the  Phipps  Institute,  who  were  charted 
as  having  abnormal  physical  signs  no  less  than  67  had  impairment  and 
broncho-vesicular  breathing  at  the  right  apex.  It  will  be  recalled  that 
in  the  adult  the  right  apex  normally  has  a  slightly  impaired  note,  pro- 
longed expiration,  and  increased  fremitus,  and  that  the  explanation  of 
this  was  pointed  out  by  Fetterolf2  as  being  due  to  close  proximity  of  the 
trachea  to  the  right  upper  lobe.  The  very  high  proportion  of  cases  in 
this  group,  with  apparent  disease  at  the  right  apex,  would  seem  to  indi- 
cate that  what  was  in  reality  a  normal  finding  was  interpreted  as  being 
pathological. 

One's  belief  in  this  is  strengthened  from  the  result  of  reports  of  111 
of  these  children  three  or  four  years  after  the  first  observation.     Of  these 

1  "Text-book  of  Human  Physiology,"  10th  ed.,  p.  391. 

2  Arch.  Int.  Med.,  Feb.,  1909. 


DISEASES    OF   THE    LUNGS  359 

111  cases  17  were  noted  as  having  a  diseased  right  apex,  and  in  2  more 
both  apices  were  supposed  to  be  affected.  At  the  time  they  were  in- 
vestigated 17  of  the  19  were  noted  as  being  in  good  health,  1  had  died  of 
tuberculosis,  and  1  still  had  some  cough.  By  some,  the  presence  of 
abnormal  physical  signs  at  the  right  apex  is  believed  to  be  due  to  enlarge- 
ment of  the  tracheo-bronchial  lymph  nodes. 

In  addition  to  the  exaggeration  of  the  breath  sounds  already  noted  the 
respiratory  sounds  in  children  are  subject  to  a  number  of  vagaries,  and  the 
younger  the  child  the  more  difficult  is  the  interpretation  of  the  auscultatory 
signs.  The  expired  air  may,  for  instance,  be  directed  into  the  pharyngeal 
vault  or  against  the  roof  of  the  mouth,  with  the  result  that  a  bronchial 
quality  of  breathing  is  heard  all  over  the  chest.  This  can  be  obviated 
if  the  child  is  old  enough  to  learn  how  to  breathe  properly.  Then  again 
in  young  children  and  infants  the  lungs  at  times  seem  to  move  inde- 
pendently of  one  another,  with  the  result  that  loud  puerile  breathing  is 
heard  over  one  side,  while  over  the  opposite  side  the  breath  sounds  are 
almost  inaudible,  and  this  condition  shifts  from  side  to  side.  This 
peculiarity  is  often  due  to  faulty  posture.  If  care  is  not  taken  to  see 
that  the  child  sits  straight,  and  that  one  or  the  other  side  is  not  held 
tense,  not  only  will  there  be  very  faint  or  nearly  absent  breath  sounds  on 
the  cramped  side,  but  in  addition  the  percussion  note  may  be  impaired, 
or  indeed  absolutely  dull.  I  have  often  demonstrated  this  fact  to 
students  and  shown  them  how  the  signs  on  the  two  sides  can  be  almost 
instantly  reversed.  This  fact  is  worth  remembering,  as  the  unwary  may 
make  a  diagnosis  of  pneumonia  or  pleural  effusion. 

Lymph  Nodes. — In  nearly  every  article  dealing  with  the  diagnosis  of 
tuberculosis  in  children  great  stress  has  been  laid  on  the  presence  of  pal- 
pably enlarged  cervical  lymph  nodes.  Indeed  in  not  a  few  instances,  in 
which  surveys  of  large  groups  of  children  have  been  made,  this  apparently 
has  been  the  only  evidence  on  which  the  diagnosis  was  made.  The  fact 
has  been  ignored  that  the  age  of  childhood  is  likewise  known  as  the 
lymphoid  age,  and  that  all  children,  irrespective  of  their  social  condition, 
have  lymph  nodes  which  are  readily  palpable.  The  enlargement  of  the 
lymph  nodes  is  not  readily  detected  until  about  the  second  year,  but 
from  then  on  until  shortly  before  or  after  the  age  of  puberty  this  is  the 
case,  although  as  the  child  approaches  adolescence  certain  groups,  such 
as  the  epitrochlear,  the  axillary,  and  the  inguinal,  tend  to  shrink  in  size 
and  become  less  easily  detected.  The  submaxillary  node  at  the  angle  of 
the  jaw  is  usually  the  largest  under  normal  conditions,  and  is  usually 
the  last  to  shrink  to  a  size  that  it  can  no  longer  be  palpated. 

To  confine  the  examination  to  one  group,  such  as  the  cervical,  and 
because  the  nodes  in  this  situation  are  palpable,  to  assume  that  it  is  an 
evidence  of  tuberculous  infection  does  not  seem  in  any  way  justifiable, 
especially  so  in  view  of  the  fact  that  all  the  lymph  nodes  of  the  body  are 
hypertrophied  according  to  adult  standards. 

If  there  exist  in  the  neck  a  single  large  node  or  a  tumor  mass  made 
up  of  a  number  of  nodes,  which  are  matted  together  and  adherent  to  the 
surrounding  tissues,  the  presumption  is  strong  that  we  have  to  deal  with 
a  tuberculous  adenitis,  and  especially  so  if  there  is  evidence  of  softening, 
or  the  overlying  skin  is  inflamed.  This,  however,  is  true  scrofula,  and 
has  nothing  to  do  with  nodes  which  vary  in  size  from  that  of  a  bean  to 


360       DISEASES   OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND   DIAPHRAGM 

a  split  pea,  or  smaller,  which  are  freely  movable,  and  which  manifest 
neither  softening  nor  inflammation. 

Ten  years  ago  children  who  were  definitely  classed  as  being  tuber- 
culous are  to-day  considered  as  belonging  to  the  so-called  pretuberculous 
group.  Such  children  are  usually  anemic,  under-nourished  and  under- 
sized; the  lymph  nodes  are  easily  palpable  and  the  von  Pirquet  or  Moro 
skin  tests  are,  as  a  rule,  positive.  The  type  is  a  familiar  one  among  the 
children  of  the  poorer  classes  although  by  no  means  limited  to  them. 
In  the  great  majority  of  these  children  the  evidences  of  ill  health  dis- 
appear if  the  living  conditions  can  be  improved  and  above  all  if  an  ade- 
quate dietary  can  be  obtained.  The  open  air  school  has  demonstrated 
very  clearly  how  quickly  these  children  react  to  improved  sanitary 
conditions. 

TUBERCULOSIS     OF    THE    TRACHEO-BRONCHIAL    LYMPH    NODES 

Of  recent  years  much  has  been  written  on  the  subject  of  enlargement 
of  the  mediastinal  lymph  nodes.  As  I  have  already  stated  a  diagnosis 
of  chronic  tuberculosis  of  the  lungs  in  children  is  now  far  less  common  than 
was  formerly  the  case.  At  the  present  time  children  presenting  obscure 
symptoms  which  may  be  tuberculous  in  origin,  are  considered  by  many 
to  be  suffering  from  a  localized  infection  of  the  tracheo-bronchial  lymph 
nodes.  The  majority  of  observers  consider  that  the  initial  lesion  in 
children  is  situated  in  these  nodes  and  that  the  invasion  of  the  lungs  is 
secondary.  Ghon,1  on  the  other  hand,  places  the  initial  lesion  in  the  lung. 
It  is  his  belief  that  the  bronchial  lymph  nodes  are  secondarily  invaded. 
Among  young  children  and  infants  who  succumb  to  tuberculosis,  infec- 
tion of  the  mediastinal  lymph  nodes  is  a  common  finding.  The  disease 
may  become  so  extensive  as  to  cause  death  without  spreading  to  other 
structures.  More  frequently,  however,  the  disease  invades  the  lungs  or 
becomes  widely  disseminated.  If  the  child  survives  this  initial  infec- 
tion, the  process  in  the  majority  of  instances  becomes  arrested.  In 
children  over  three  years  of  age  fibrous  and  calcareous  changes  very 
frequently  take  place. 

Symptoms. — The  symptomatology  of  this  condition  is  very  indefinite. 
In  the  majority  of  cases  in  which  there  is  reason  to  believe  that  the 
tracheo-bronchial  nodes  are  tuberculous  the  child  is  anemic,  frail  and 
obviously  out  of  health.  Susceptibility  to  acute  colds  may  in  some 
instances  be  due  to  enlargement  of  these  nodes.  There  may  be  a  brassy 
cough,  some  dyspnea  and  at  times  thoracic  pain,  especially  in  the  inter- 
scapular region.  Rupture  of  an  enlarged  gland  into  one  of  the  surrounding 
structures  occasionally  occurs. 

Physical  Signs. — The  physical  signs  are  quite  as  inconclusive  as  the 
symptoms.  Enlargement  of  the  veins  over  the  upper  part  of  the  chest 
is  cited  as  one  of  the  evidences  of  enlarged  mediastinal  glands.  On 
percussion  dulness  in  the  first  and  second  interspaces  close  to  the  ster- 
num and  dulness  over  and  to  either  side  of  the  upper  thoracic  vertebra 
is  ascribed  by  most  authorities  as  being  quite  constantly  present.  The 
percussion  changes  are  usually  more  marked  on  the  right  side.  On 
auscultation  Eustace  Smith's  sign  is  occasionally  encountered  but  the 

1  "The  Primary  Lung  Focus  of  Tuberculosis  in  Children,"  Trans,  by  Barty  King, 
1916. 


DISEASES    OF    THE    LUNGS  361 

frequency  of  venous  hums  at  the  root  of  the  neck  in  healthy  children 
renders  this  sign  of  questionable  value. 

The  one  sign  upon  which  the  most  emphasis  has  been  laid  is  that 
described  by  D'Espine.1  This  sign  consists  of  a  prolongation  of  the 
whispered  voice  over  the  upper  dorsal  vertebrae;  occasionally  it  is  heard 
as  low  as  the  eighth  dorsal  vertebra.  It  is  elicited  by  having  the  patient 
whisper  "one,  two,  three,"  "three,  thirty-three"  or  repeat  the  word 
"tree."  The  distinctive  quality  of  the  sign  is  the  prolongation  of  the 
final  "e,"  for  an  appreciable  time  after  the  voice  stops.  Some  believe 
D'Espine's  sign  is  pathognomonic  of  enlarged  tracheo-bronchial  lymph 
nodes;  others,  while  attaching  great  importance  to  its  presence,  state 
that  it  is  heard  at  times,  in  the  absence  of  any  such  enlargement.  Morse2 
in  a  study  of  666  children  of  the  wealthy  and  well-to-do  classes  was  able 
to  elicit  the  sign  in  but  40  (6  per  cent.). 

Although  not  infallible,  an  X-ray  examination  is  the  most  certain 
method  of  detecting  enlargement  of  this  group  of  lymph  nodes. 

Diagnosis. — Occasionally  a  child  is  seen  in  which  the  symptoms,  the 
physical  signs  and  the  radiograph  point  almost  conclusively  to  this  con- 
dition. But  in  most  instances  neither  the  symptoms  nor  the  physical 
signs  are  distinctive.  In  delicate  children,  and  especially  in  those  who 
give  a  history  of  exposure  to  the  disease,  an  X-ray  examination  should  be 
made.  It  is  to  be  borne  in  mind,  however,  that  any  of  the  acute  infec- 
tions are  apt  to  cause  enlargement  of  the  lymph  nodes  and  that  this 
enlargement  may  persist.  It  is,  therefore,  evident  that  while  the  X-rays 
will  show  enlargement  of  the  lymph  nodes  they  do  not  indicate  the 
etiological  factor. 

Although  the  diagnosis  of  enlargement  of  the  mediastinal  lymph 
nodes  in  children  is  a  common  one,  my  own  experience,  checked  up  by 
radiographic  examinations,  is  that  the  condition  is  less  frequent  than 
most  observers  claim  and  that  the  enlargement,  when  present,  lacks  the 
serious  significance  many  authors  attach  to  it. 

ACUTE  TUBERCULOSIS  OF  THE  LUNGS 

Galloping  Consumption,  Phthisis  Florida. — In  contrast  to  the  chronic 
type  of  the  disease  pulmonary  tuberculosis  occurs  also  in  an  acute  form 
of  which  there  are  two  types,  the  penumonic  and  the  broncho-pneumonic. 
In  the  chronic  form  of  the  disease  the  progress  is  slow  and  the  duration  of 
the  disease  usually  is  measured  by  years.  In  the  acute  types,  on  the  other 
hand,  the  invasion  is  rapid  and  widespread  and  may  end  fatally  within 
a  few  weeks,  particularly  when  it  occurs  in  children.  In  adults  the  course 
of  the  disease  is  more  often  subacute  and  may  be  prolonged  for  five  or  six 
months  or  even  longer.  Occasionally  what  promises  in  the  beginning  to 
be  an  acute  process  subsides  and  undergoes  arrest  or  develops  into  the 
chronic  ulcerative  type  of  the  disease. 

The  Broncho-pneumonic  Form 

This  is  the  most  frequent  and  the  most  characteristic  form  of  tuber- 
culosis in  infants  and  young  children,  and  is  the  one  which  at  this  age 

1  Bull.  Acad,  de  Med.,  1907,  lviii,  142-14(3.      , 
-  Ain.  Jour.  Dis.  Children,  April,  1916. 


362       DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

usually  causes  death  (Holt).  Acute  tuberculosis  is  not  uncommonly 
the  sequel  to  an  attack  of  measles  or  whooping  cough.  In  negroes,  acute 
or  subacute  pulmonary  tuberculosis,  particularly  of  the  broncho-pneu- 
monic type,  is  relatively  common.  Among  adults  of  the  white  races 
acute  broncho-pneumonic  phthisis  is  relatively  infrequent.  It  is  most 
apt  to  occur  in  young  females  or  in  those  with  a  strong  hereditary 
predisposition. 


Fig.  263. — This  specimen  obtained  from  a  young  colored  girl  shows  the  acute  broncho- 
pneumonic  type  of  disease.  Lung  breaking  down  rapidly  and  forming  large  ragged 
cavities.     Dense  infiltration  in  lower  lobe. 

In  cases  of  chronic  ulcerative  tuberculosis  an  acute  broncho-pneumonic 
process  is  not  infrequently  engrafted  upon  the  chronic  process  as  the  result 
of  the  aspiration  of  the  contents  of  a  cavity  or  the  aspiration  of  blood 
following  an  hemoptysis. 

Morbid  Anatomy. — The  commonly  accepted  teaching  has  been  that 
in  children  the  primary  focus  is  one  of  the  peribronchial  lymph  nodes  and 
that  infection  of  the  lung  is  brought  about  by  the  rupture  of  a  caseous  area 
into  a  bronchus  near  the  hilus.  Ghon,  however,  asserts  that  the  reverse  is 
true.  He  believes,  as  a  result  of  careful  anatomical  studies,  that  the  pri- 
mary focus  is  in  the  lung  and  that  the  peribronchial  nodes  are  involved 


DISEASES    OF    THE    LUNGS 


363 


secondarily.     In  children  both  lungs  are  involved  but  usually  one  is  much 
more  so  than  the  other. 

In  adults  an  old  quiescent  focus  or  partially  healed  cavity  may  sud- 
denly become  active  and  rapidly  invade  a  portion  of  or  all  of  one  lung. 
On  section  the  lung  is  moist  and  seen  to  be  studded  with  areas  of  various 
sizes  which  are  usually  ranged  around  the  bronchi  "like  clusters  of  grapes 
about  the  stem."  The  patches  may  be  very  small  in  which  case  they  are 
gray  or  semitranslucent,  or  they  may  be  quite  large  as  the  result  of  the 
coalescence  of  several  areas.  The  latter  are  usually  grayish  red  or 
yellowish  white  in  color. 


Fig.  264. — Broncho-pneumonic  type  of  tuberculosis.     Rapid  breaking  down  of  tissue  in 
right  lung.     Chronic  fibroid  condition  at  left  apex  which  is  probable  source  of  infection. 

The  fusion  of  a  number  of  contiguous  patches  often  gives  rise  to  large 
caseous  foci  in  which  softening  takes  place  very  rapidly.  In  the  very 
acute  cases  death  may  ensue  before  softening  and  breaking  down  takes 
place  but  in  the  subacute  cases  cavity  formation  is  usually  the  rule. 
Between  the  caseous  areas  the  lung  tissue  may  be  crepitant  or  it  may  be 
grayish  red  and  infiltrated  with  a  serofibrinous  or  gelatinous  material 
(gelatinous  pneumonia). 


364 


DISEASES   OF   THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 


The  disease  spreads  rapidly.  The  individual  foci  increase  in  size 
and  by  coalescing  with  contiguous  patches  form  large  caseous  areas  which 
show  little  or  no  tendency  to  fibrosis.  As  a  result  caseation,  softening 
and  the  formation  of  ragged,  irregular-shaped  cavities  are  common 
(Figs.  263  and  264). 

Symptoms. — The  disease  may  manifest  itself  abruptly  with  a  chill 
or  a  succession  of  chills.  The  temperature  rises  quickly  and  the  patient 
has  every  appearance  of  being  acutely  ill.     In  children  the  initial  stage 


Fig.  265. — Caseous  pneumonia. 

differs  hardly  at  all  from  that  seen  in  ordinary  broncho-pneumonia.  At 
times  the  first  evidence  of  trouble  is  an  hemoptysis.  More  often  the 
onset  is  more  or  less  insidious.  The  patient  has  a  slight  cough,  some 
elevation  of  temperature,  malaise  and  pains  in  the  limbs.  In  addition 
he  has  no  appetite,  feels  weak,  and  has  no  ambition  to  go  about  his 
daily  duties. 

In  a  relatively  short  time  the  symptoms  become  well  marked.  The 
temperature  becomes  high  and  continuous  in  type  with  an  occasional 
intermission  or  remission   (see  Figs.  247  and  248),  the  cheeks  have  a 


DISEASES    OF    THE    LUNGS 


365 


hectic  flush  and  the  skin  becomes  burning  hot.  Emaciation  is  usually 
very  marked  and  within  a  few  weeks  the  patient  may  be  but  a  shadow 
of  his  former  self.  Severe  toxemia  manifests  itself  by  chills  and  drench- 
ing sweats.  The  cough  becomes  progressively  worse  and  the  sputum 
more  and  more  abundant.  The  latter  is  at  first  mucoid  but  soon  be- 
comes yellowish  or  greenish  in  color  and  may  be  streaked  with  blood. 
Tubercle  bacilli  are  usually  abundant. 

As  the  disease  progresses  the  pulse  becomes  more  and  more  rapid 
and  the  respiration  is  also  greatly  accelerated. 


Fig.  266. — Caseous  pneumonia.     Primary  focus  a  cavity  at  the  apex. 

Physical  Signs. — In  common  with  the  chronic  type  the  acute  form  of 
the  disease  almost  invariably  appears  first  at  the  apices  or  if  a  large  por- 
tion of  the  lung  is  invaded  the  signs  are  most  marked  at  the  summit  of 
the  lungs.  At  the  beginning  rales  such,  as  occur  in  acute  bronchitis  may 
be  heard  over  one  or  both  lungs.  Sooner  or  later  the  evidences  of  in- 
filtration become  apparent.  There  is  clulness  on  percussion,  increased 
tactile  fremitus  and  broncho-vesicular  breathing.  Mixed  rales  are  heard 
especially  the  fine  crackling  variety  after  coughing.     Quite  often  there 


366      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

is  also  present  a  pleural  friction  rub.     If  the  caseous  areas  break  down 
and  empty  through  a  bronchus  the  usual  signs  of  cavity  are  present. 

In  children  presenting  the  symptoms  of  ordinary  broncho-pneumonia 
it  is  well  to  remember  that  a  preponderance  of  the  physical  signs  at 
the  apices  or  high  in  the  axillae  point  to  a  tuberculous  origin  of  the 
trouble. 

The  Pneumonic  or  Lobar  Form 

Acute  pneumonic  phthisis  is  a  rare  condition.  The  subacute  form, 
however,  is  relatively  common.  The  latter  may  terminate  fatally  in  the 
course  of  a  few  months ;  the  acute  symptoms  may  subside  and  the  lesion 
remain  localized;  or  it  may  pass  into  the  chronic  progressive  type. 

The  lobar  type  of  the  disease  is  very  rare  in  children  being  met  with, 
as  a  rule,  in  adults.  While  it  may  have  its  origin  in  a  tuberculous  focus 
outside  of  the  lungs  the  usual  starting  point  is  an  old  chronic  lesion  at 
the  apex  which  suddenly  becomes  active. 

Morbid  Anatomy. — The  lesion  may  involve  a  portion  of  the  lobe 
(Fig.  265),  an  entire  lobe  or  even  the  entire  lung.  The  affected  portion 
may  be  completely  consolidated  there  being  no  healthy  pulmonary  tissue 
remaining.  The  weight  of  the  lung  is  greatly  increased.  Section  through 
the  diseased  lung  shows  large  caseous  areas  which  are  smooth,  dry,  air- 
less and  of  a  yellow,  grayish-white  or  yellowish-white  color.  The  affected 
portion  cuts  like  a  piece  of  cheese.  In  some  instances  the  cut  section  is 
granular  and  presents  a  grayish-white  mottled  appearance  due  to  con- 
glomerate caseous  areas  and  consolidated  hyperemic  patches  of  pul- 
monary tissue.  Just  as  in  the  broncho-pneumonic  form  there  is  little 
or  no  evidence  of  the  formation  of  fibrous  tissue.  This  is  especially 
noticeable  if  a  cavity  forms.  Instead  of  a  limiting  fibrous  membrane, 
such  as  is  seen  in  the  chronic  type  of  the  disease,  the  wall  is  composed  of 
ragged,  necrotic  tissue  (Fig.  266). 

The  overlying  pleura  usually  shows  inflammatory  changes  and  a 
fibrinous  exudate.  The  peri-bronchial  lymph  nodes  are  swollen  and 
often  caseous. 

Symptoms. — The  onset  in  this  type  of  the  disease  is  nearly  always 
abrupt.  Quite  often  the  individual  is  known  to  have  an  old  localized 
tuberculous  process  at  one  apex  but  not  uncommonly  there  has  been  no 
evidence  of  ill  health  and  the  family  history  is  good. 

The  onset  is  practically  identical  with  that  of  lobar  pneumonia.  The 
patient,  after  exposure  to  cold,  is  suddenly  seized  with  a  chill,  and  severe 
pain  in  the  side.  The  temperature  rises  rapidly  and  is  continuous  in 
type  (see  Fig.  249).  There  is  a  suppressed  cough,  the  sputum  is  blood- 
tinged  or  even  typically  rusty  in  character  and  the  respiratory  rate  is 
quickened.  No  suspicion  is  entertained  that  the  condition  is  other  than 
a  lobar  pneumonia  until  the  duration  of  the  latter  has  been  exceeded  and 
no  crisis  occurs.  In  addition  the  temperature  becomes  hectic  in  type 
and  the  sputum  mucopurulent.  Tubercle  bacilli  usually  can  be  demon- 
strated at  this  time.  The  patient  suffers  from  chills  and  sweating  and 
also  emaciates  rapidly.  A  fatal  issue  may  occur  in  four  or  five  weeks 
or  the  condition  may  become  subacute  and  be  prolonged  for  months.  If 
only  a  limited  portion  of  a  lobe  is  involved  the  acute  symptoms  may 
subside  and  the  lesion  becomes  arrested  or  slowly  progressive. 


DISEASES    OF    THE    LUNGS  367 

Physical  Signs. — The  physical  signs  of  acute  pneumonic  phthisis 
are  always  found  at  one  or  the  other  apex  of  the  lung;  never  at  the  bases. 
They  differ  in  no  particular  from  those  occurring  in  lobar  pneumonia, 
namely,  increased  tactile  fremitus,  dulness  on  percussion,  exaggeration 
of  the  voice  sounds,  bronchial  breathing  and  fine  crackling  rales.  Some 
observers  point  out  that  the  breath  sounds  in  tuberculous  pneumonia 
are  more  often  suppressed  and  distant  than  in  the  croupous  variety  and 
that  this  is  of  diagnostic  significance. 

Later  in  the  disease  there  may  be  evidences  of  breaking  down  of  the 
lung  at  the  apex.  At  first  large  moist  rales  are  heard;  later  there  may  be 
signs  of  a  cavity. 

Diagnosis. — There  is  no  doubt  that  the  acute  forms  of  tuberculosis 
are  very  frequently  mistaken  for  lobar  pneumonia.  The  acute  onset, 
the  high  continuous  fever,  pain  in  side,  and  blood-streaked  sputum  to- 
gether with  physical  signs  indicating  partial  or  complete  consolidation 
are  responsible  for  this.  In  many  such  cases  the  acute  process  subsides 
in  a  few  weeks  and  the  patient  apparently  recovers;  in  others  a  tubercu- 
losis is  said  to  have  developed  after  the  pneumonia.  It  is  to  be  remem- 
bered that  tuberculosis  very  often  undergoes  an  acute  exacerbation  last- 
ing for  a  few  weeks  and  again  becomes  quiescent.  Of  4466  cases  seen  at 
the  Phipps  Institute  no  less  than  17.77  per  cent,  gave  a  history  of  having 
had  an  attack  of  pneumonia.  How  many  of  these  attacks  were  in 
reality  an  acute  exacerbation  of  the  tuberculosis  is  problematical,  but  it 
is  fair  to  assume  that  a  considerable  number  were  of  that  nature. 

While  it  is  often  impossible  during  the  acute  stage  to  differentiate 
between  lobar  pneumonia  and  pneumonic  phthisis  the  following  points 
are  helpful:  (1)  A  history  of  tuberculosis  in  the  family;  (2)  a  knowledge 
of  the  existence  of  an  old  tuberculous  lesion;  (3)  a  longer  duration  in  the 
case  of  pneumonic  phthisis;  (4)  herpes  are  common  in  croupous  pneu- 
monia and  rare  in  the  tuberculous  form;  (5)  a  leukocytosis  is  common 
in  lobar  pneumonia;  and  (6)  the  location  of  the  lesion.  Croupous  pneu- 
monia most  frequently  involves  the  lower  lobes  but  may  occur  in  the 
upper  lobes.  As  a  rule  acute  tuberculosis  is  limited  to  or  most  marked 
in  the  upper  lobes.  If,  however,  there  is  a  lesion  already  in  the  upper 
lobe  a  rapid  invasion  of  the  lower  lobe  may  take  place  with  symptoms 
and  physical  signs  similar  to  those  of  lobar  pneumonia.  The  latter 
group  offer  the  greatest  difficulty  and  it  is,  as  a  rule,  not  possible  to 
tell  which  disease  is  present  until  several  weeks  have  elapsed.  If  the 
symptoms  and  physical  signs  persist  it  can  be  assumed  with  certainty 
that  the  lesion  is  tuberculous  in  nature.  When  the  upper  lobes  are  in- 
volved, tuberculosis  should  always  be  kept  in  mind,  especially  if  there  is 
a  family  history  of  tuberculosis  or  the  patient  gives  a  history  of  having 
been  in  poor  health  (see  also  p.  412). 

FIBROID  PHTHISIS 

In  certain  instances  tuberculosis  assumes  a  very  chronic  form  char- 
acterized by  extensive  fibroid  changes  in  the  affected  lung.  The  arrest 
of  a  tuberculous  process  is  largely  due  to  the  formation  of  fibrous  tissue 
about  the  lesions  and  even  in  those  cases  in  which  the  disease  progresses 
the  rapidity  of  its  advance  is  determined  by  the  amount  of  fibrosis  which 
takes  place.     In  the  acute  types  of  pulmonary  tuberculosis  in  which  the 


368       DISEASES   OF   THE  BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

course  of  the  disease  is  relatively  short  and  the  pulmonary  lesions  wide- 
spread, there  is  little  or  no  evidence  of  fibroid  changes.  The  opposite 
extreme  is  encountered  in  the  type  of  the  disease  under  discussion. 
Here  the  formation  of  fibroid  tissue  far  exceeds  what  is  needed,  thus 
giving  rise  to  pulmonary  fibrosis  with  its  results. 

Clarke,  Hadley  and  Chaplin  in  their  authoritative  monograph  on  the 
subject  of  Fibroid  Phthisis  distinguished  three  forms:  (1)  Tuberculo- 
fibroicl  disease,  a  condition  which  is  primarily  tuberculous  but  in  which 
there  is  an  overgrowth  of  fibrous  tissue;  (2)  fibro-tuberculous  disease,  a 
condition  which  is  primarily  a  pure  fibrosis  but  later  becomes  tuberculous; 
and  (3)  pure  fibroid  disease  of  the  lung. 

The  first  type  may  from  the  beginning  be  characterized  by  an  exces- 
sive amount  of  fibrous  tissue  or  the  chronic  ulcerative  type  of  tuberculosis 
may  change  into  the  fibroid  type.  In  the  latter  instance  a  single  iso- 
lated cavity  at  the  apex  may  be  surrounded  by  a  thick,  dense  wall  of 
fibroid  tissue  involving  both  the  surrounding  pulmonary  tissue  and 
the  pleura.  In  a  case  seen  at  the  Phipps  Institute  a  large  apical  cavity 
was  surrounded  by  dense  cartilaginous  material  which  in  places  was  over 
an  inch  in  thickness.  The  fibrous  process  may  be  limited  to  the  apex  or 
gradually  involve  the  entire  lung. 

In  regard  to  the  fibro-tuberculous  and  pure  fibroid  types  it  has  been 
objected  that  they  are  only  examples  of  "phthisis  of  which  the  history 
has  been  forgotten."  Pure  fibrosis  of  the  lung,  although  rare,  does, 
however,  exist.  Two  excellent  examples  of  the  disease  have  been  seen 
at  the  Phipps  Institute.  The  SA^mptoms  and  physical  signs  of  fibroid 
phthisis  differ  in  no  particular  from  those  encountered  in  pulmonary 
fibrosis  or  cirrhosis  of  the  lung.  The  sections  on  Bronchiectasis  and 
Pulmonary  Fibrosis  should  be  consulted  in  connection  with  this  subject. 

ACUTE  MILIARY  TUBERCULOSIS 

This  form  of  tuberculosis  requires  special  consideration  because  of 
its  anatomical  relations  and  clinical  manifestations.  "The  term  'miliary 
tuberculosis'  is  applied  to  the  appearance  of  numerous  small,  gray  or 
grayish-red  tuberculous  nodules  about  the  size  of  a  millet-seed  and 
approximately  at  the  same  degree  of  development  in  an  organ,  especially 
the  lung,  or  in  only  a  certain  portion  of  the  lung.  By  general  miliary 
tuberculosis  we  designate  the  fairly  regular  distribution  of  such  nodules 
in  all  or  several  of  the  organs  of  the  bod}',  particularly  the  lung,  liver, 
spleen,  kidney,  brain,  bone-marrow,  etc.  As  a  rule,  the  disease  is  acute 
and  characterized  by  a  tumultuous  course,  terminating  in  death  usually 
in  a  few  weeks"  (Cornet). 

Etiology. — The  modern  conception  of  miliary  tuberculosis  dates  from 
the  statement  made  by  Buhl  (1856),  that  miliary  tuberculosis  is  a  specific 
infectious  disease,  the  miliary  nodule  bearing  the  same  relation  to  a 
caseous  focus  as  the  metastatic  abscesses  in  pyemia  have  to  the  primary 
focus  of  suppuration.  Some  years  later  Weigert  furnished  the  proof  as 
to  the  manner  in  which  the  tubercle  bacilli  are  disseminated.  This  may 
be  brought  about  by  direct  invasion  of  the  walls  of  blood-vessels  or  the 
thoracic  duct  or  by  the  rupture  into  one  of  these  vessels  of  an  adjacent 
tuberculous  focus.  Miliary  tuberculosis  occurring  under  natural  con- 
ditions is  analogous  to  experimental  tuberculosis  in  which  an  enormous 


DISEASES    OF    THE    LUNGS  369 

number  of  tubercle  bacilli  are  injected  directly  into  the  vein  of  an 
animal.  In  both  instances  the  body  is  suddenly  overwhelmed.  When 
the  lungs  are  specially  affected  it  is  generally  the  result  of  a  pulmonary 
lesion  or  a  caseous  tracheal  or  bronchial  lymph  node,  which  has  broken 
down  and  discharged  its  contents  into  a  branch  of  the  pulmonary  vein. 
In  the  more  widely  disseminated  form  of  the  disease  the  most  frequent 
source  of  the  infection  is  the  thoracic  duct.  Longcope1  in  a  study  of  19 
typical  cases  of  generalized  acute  miliary  tuberculosis  found  in  14  more 
or  less  extensive  tuberculosis  in  the  thoracic  duct,  usually  with  caseous 
nodules.  Ullom2  examined  the  thoracic  duct  in  17  cases  of  chronic 
pulmonary  tuberculosis  but  found  neither  tubercles  in  the  structure  nor 
tubercle  bacilli  in  the  contents  of  the  ducts. 

Both  the  site  of  the  initial  lesion  and  the  localization  of  the  miliary 
nodules  vary  greatly  in  different  cases,  as  can  be  seen  from  the  following- 
examples  which  have  come  to  my  notice.  In  one  instance  a  widespread 
dissemination  followed  the  rupture  of  a  caseous  lymph  node  into  the 
thoracic  duct  in  a  case  with  old  hip-joint  disease;  in  another  the  miliary 
nodules  were  confined  entirely  to  the  abdominal  organs,  the  primary 
source  being  a  single  tuberculous  ulcer  in  the  ileum;  in  another  the  nodules 
were  limited  to  one  lung  the  source  of  the  infection  being  an  old  cavity 
surrounded  by  a  dense  cicatricial  wall;  in  three  instances  tuberculosis 
of  the  testicles  was  followed  by  miliary  tuberculosis,  the  dominant  feature 
being  localization  in  the  meninges. 

The  relation  which  pulmonary  tuberculosis  bears  to  the  acute  miliar}" 
form  of  the  disease  is  an  interesting  one.  At  first  sight  it  would  seem 
reasonable  to  believe  that  this  would  be  the  most  frequent  predisposing 
factor.  As  a  matter  of  fact  widespread  dissemination  is  unusual  and 
while  miliary  tubercles  in  parts  of  the  lung  previously  free  from  disease 
are  frequently  found  at  autopsy  their  presence  is  often  overlooked  during 
life.  It  is  of  course  recognized  that  in  all  cases  of  chronic  pulmonary 
tuberculosis  most  of  the  organs  of  the  body  will  show,  either  macroscopic- 
ally  or  microscopically,  small  nodules,  but  which,  in  the  strict  sense  of 
the  term,  are  not  miliary  tubercles..  They  point  to  a  hematogenous 
dissemination  shortly  before  death.  These  nodules  are  possibly  due  in 
part  to  dead  tubercle  bacilli  which  are  known  to  produce  such  changes. 
Histologically  these  nodules  are  evidently  of  recent  formation.  In  a 
study  of  37  livers  from  phthisical  subjects  Ullom3  found  small  tuberculous 
foci  present  in  30  or  81  per  cent.  Walsh4  obtained  similar  results  in  a 
study  of  the  kidneys. 

Although  generalized  miliary  tuberculosis  is  comparatively  infrequent 
as  a  terminal  manifestation  of  pulmonary  tuberculosis,  miliary  tuber- 
culosis limited  to  the  lungs  or  the  meningeal  type  of  the  disease  are 
not  uncommon.  Miliary  tuberculosis  of  the  lungs  alone  is  most  apt  to 
develop  in  cases  with  an  obsolete  quiescent  lesion,  especially  if  this  lesion 
is  caseous.  The  danger  is  far  less  if  the  lesion  has  become  encapsulated 
with  fibrous  tissue.  The  meningeal  type  of  miliary  tuberculosis  is  occa- 
sionally the    terminal  manifestation   of  phthisis.      Brown5  states    that 

1  Bulletin  Ayer  Clinical  Laboratory,  Pa.  Hospital,  Xo.  3,  1906. 

2  5th  Annual  Report,  Phipps  Institute,  1908. 

3  2d  Annual  Report,  Phipps  Institution,   1905. 

4  3d  Annual  Report,  Phipps  Institute,  1906: 

5  Osler's    "  [Modern  Medicine,'-  vol.  iii.  1st  ed'.,  p.  302. 


370      DISEASES   OF  THE  BRONCHI,    LUNGS,   PLEURA,   AND   DIAPHRAGM 

tuberculous  meningitis  was  the  ultimate  cause  of  death  in  8  of  352 
males  (2.27  per  cent.)  and  in  3  of  322  females  (0.93  per  cent.)  discharged 
from  the  Adirondack  Cottage  Sanatorium. 

Miliary  tuberculosis  may  occur  at  any  age  period  but  is  far  more 
common  in  early  life  than  later.  Of  the  exciting  causes  the  acute  in- 
fectious diseases  are  the  most  important,  especially  measles  and  whooping 
cough.  Typhoid  fever  is  often  cited  as  a  predisposing  cause  but  in  the 
vast  majority  of  such  cases  there  has  been  an  error  in  diagnosis.  As  will 
be  shown  later,  enteric  fever  and  the  typhoid  form  of  miliary  tuberculosis 
are  differentiated  only  with  the  greatest  difficulty.  Acute  dissemination 
is  not  infrequent  following  an  operation  on  a  tuberculous  bone  or  joint. 
Operations  on  individuals  with  frank  pulmonary  tuberculosis  are  rarely 
followed  by  miliary  tuberculosis.  There  may  be,  however,  an  exacerba- 
tion of  the  disease.  In  such  cases  the  dissemination  in  the  lungs  is  peri- 
bronchial in  character  and  is  due  to  the  insufflation  of  tuberculous 
material.  If  this  occurs  it'is  practically  always  due  to  ether;  other  forms 
of  anesthesia  are  well  borne  by  phthisical  subjects.  Among  other  pre- 
disposing causes  may  be  mentioned  traumatic  injuries,  pregnancy,  chronic 
debilitating  affections,  or  any  factor  which  tends  to  reduce  the  vitality, 
such  as  grief  or  worry.  Occasionally  miliary  tuberculosis  follows  the 
rapid  absorption  of  a  pleural  exudate. 

It  is  difficult  to  estimate  the  frequency  of  this  type  of  tuberculosis. 
It  is  encountered  far  more  often  in  general  hospitals  than  in  institutions 
which  care  exclusively  for  tuberculous  patients. 

Morbid  Anatomy. — Every  case  of  miliary  tuberculosis,  whether 
widely  disseminated  or  limited  to  a  single  organ,  has  its  origin  in  an 
old  caseous  focus.  At  autopsy  this  may  be  easily  demonstrated  or  it 
may  be  so  small  or  so  situated  in  some  portion  of  the  body  not  routinely 
examined,  as  to  .escape  detection.  Anatomically  the  disease  is  character- 
ized by  the  presence  of  countless  miliary  nodules  varying  in  size  from 
that  of  a  pinhead  to  a  millet-seed  (Fig.  .267).  The  tubercles  may  be 
confined  or  at  least  most  marked,  in  a  single  organ  or  they  may  invade 
nearly  every  portion  of  the  body.  The  organs  which  are  especially 
vulnerable  are  the  lungs,  liver,  spleen,  and  kidneys,  the  serous  membranes 
and  often  the  choroid.  For  some  reason  the  pancreas,  the  skeletal 
muscles  and  the  lymph  nodes  are  very  resistant  and  rarely  show  the 
presence  of  tubercles. 

The  predominance  of  tubercles  in  certain  organs  will  often  give  the 
clue  as  to  the  site  of  the  original  focus.  Thus  if  the  liver  is  most  involved 
the  primary  lesion  is  in  the  area  drained  by  the  portal  vein ;  if  the  tubercles 
are  most  numerous  in  the  spleen,  liver  and  kidney  the  infection  has 
probably  been  carried  by  the  pulmonary  veins;  uniform  distribution 
throughout  both  lungs  points  to  the  thoracic  duct  or  one  of  the  systemic 
veins.  In  the  pulmonary  type  the  demonstration  of  an  old  lesion  in  the 
lungs  is  usually  an  easy  matter. 

The  most  recent  nodules  consist  of  minute  grayish,  semitransparent 
points.  If  several  eruptions  have  taken  place,  the  tubercles  will  show 
variations  in  size  and  color.  The  older  nodules  are  larger  with  greyish- 
yellow,  yellowish-white  centers.  Microscopically  many  minute  tubercles 
may  be  demonstrated  which  cannot  be  recognized  by  the  naked  eye. 
The  affected  organs  are  usually  increased  in  size. 

The  lungs  are  larger  than  normal  and  intensely  hyperemic.     On  sec- 


DISEASES    OF    THE    LUNGS 


371 


tion  the  cut  surface  appears  dark  red  and  granular  and  the  nodules  feel 
hard.  When  the  condition  is  secondary  to  chronic  pulmonary  tubercu- 
losis of  the  lungs  in  adults  the  nodules  are  less  sharply  defined  and  tend 
to  coalesce.  The  nodules  are  always  most  numerous  in  the  immediate 
neighborhood  of  the  original  focus  and  tend  to  diminish  in  number  as 
the  base  of  the  lung  is  reached.  In  children,  on  the  other  hand,  the  pul- 
monary nodules  are  discrete  and  thickly  and  uniformly  distributed 
throughout  the  lungs. 


Fig.  267. — Miliary  tuberculosis. 


The  bronchi  are  inflamed  and  in  children  especially  the  bronchial 
lymph  nodes  are  enlarged  and  usually  caseous.  The  pleura  may  be 
extensively  infiltrated  with  discrete  miliary  granulations.  If  the  disease 
is  widespread  the  peritoneum  and  meninges  are  also  studded  with 
tubercles.  The  presence  of  choroidal  tubercles  is  of  some  clinical 
interest. 

Symptoms. — The  clinical  manifestations  of  miliary  tuberculosis  are 
extremely  varied  (Figs.  268  and  269).  In  some  instances  the  picture 
is  that  of  an  acute  general  infection  without  localizing  symptoms;  in 
others  there  are  marked  local  symptoms,   as  for  instance,   when  the 


372      DISEASES   OF   THE  BROXCHI,    LUNGS,    PLEITRA,   AXD   DIAPHRAGM 

meninges  are  involved.  The  symptoms  depend  on  two  factors:  (1) 
a  toxemia  due  to  the  absorption  of  tubercle  proteins;  and  (2)  to  the 
presence  of  the  tubercles  in  the  various  organs.     In  the  vast  majority 


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DISEASES    OF    THE    LUNGS 


373 


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through  the  various  organs  and  during  life  the  course  of  the  disease  was 
protracted,  lasting  from  three  to  nine^months. 

1  hoc.  cit. 


374      DISEASES   OP  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

Clinically  the  cases  are  usually  grouped  as  follows:  (1)  the  typhoid 
form  in  which  the  picture  is  that  of  an  acute  general  infection;  (2)  the 
pulmonary  form;  and  (3)  theoneni,ngeal  form.  It  is  to  be  understood 
that  this  classification  is  somewhat  arbitrary  and  that  in  some  instances 
the  typhoid  form  will  show  in  the- terminal  stage  evidences  of  localization 
in  the  lungs  or  the  meninges  or  both. 

The  Typhoid  Form 

The  onset  is  usually  insidious  and  the  history  is  often  almost  identical 
with  that  obtained  in  cases  of  typhoid  fever.  There  is  an  initial  period 
in  which  the  patient  complains  of  malaise,  headache,  and  anorexia. 
Digestive  disturbances  are  often  present  and  there  may  be  some  cough. 
The  temperature  is  elevated  and  for  some  days  may  closely  resemble  the 
type  of  fever  seen  in  typhoid  cases.  In  the  great  majority  of  cases,  how- 
ever, the  temperature  is  characterized  by  its  irregularity.  The  remissions 
are  much  more  marked  than  in  typhoid  fever  usually  amounting  to  two 
or  three  degrees.  In  some  instances  the  temperature  is  remittent  and 
occasionally  there  is  little  or  no  fever.  If  the  temperature  chart  is  care- 
fully examined  it  will  often  be  found  that  the  temperature  is  inverted 
from  time  to  time,  that  is  the  daily  rise  in  the  fever  occurs  in  the  morning 
and  the  drop  in  the  evening.  The  pulse  is  rapid  and  weak  but  seldom 
dicrotic.  An  increase  in  the  respiratory  rate  is  usually  present.  As  the 
disease  progresses  the  tongue  becomes  dry  and  the  lips  and  teeth  are 
covered  with  sordes.  Emaciation  is  usually  marked.  Nervous  symp- 
toms are  often  prominent  and  consist  of  restlessness,  delirium,  subsultus, 
hyperasthesia  and  a  tendency  to  mental  torpor  and  coma.  Meteorism 
is  frequently  present  and  there  may  be  diarrhea.  Occasionally  blood  is 
present  in  the  stools.  The  general  appearance  of  the  patient  and  the 
symptoms  are  essentially  the  same  as  those  occurring  in  cases  of  toxemia 
from  any  cause. 

The  physical  examination  may  furnish  but  little  information  in  the 
beginning  or  indeed  throughout  the  course  of  the  disease.  The  heart 
sounds  are  rapid  and  weak  and  the  first  sound  may  closely  resemble  the 
second.  The  lungs  may  show  no  abnormality  or  the  presence  of  a  more 
or  less  diffuse  bronchitis.  A  marked  increase  in  the  respiratory  rate 
should  arouse  one's  suspicions  as  to  the  presence  of  pulmonary  mischief. 
Cheyne-Stokes  breathing  is  occasionally  present  in  the  late  stages  of  the 
disease.  Slight  enlargement  of  the  spleen  can  often  be  made  out. 
The  presence  of  choroidal  tubercles  is  often  cited  as  an  important  diag- 
nostic sign.  They  should  always  be  looked  for  in  suspected  cases  of 
miliary  tuberculosis  but  it  is  only  rarely  that  their  detection  confirms 
the  diagnosis.  Very  often  in  miliary  tuberculosis  small  reddish  and 
slightly  elevated  spots  appear  on  the  skin.  Although  they  have  a  super- 
ficial resemblance  to  the  rose  spots  seen  in  typhoid  fever  they  do  not  come 
out  in  successive  crops  and  in  addition,  they  lack  the  other  characteristics 
of  the  true  typhoid  eruption.  A  petechial  eruption,  appearing  especially 
about  the  wrists  often  occurs  in  the  late  stages.  Rarely  jaundice  occurs 
if  there  is  extensive  involvement  of  the  liver.  I  have  seen  one  such  case. 
The  urine  may  show  traces  of  albumen.  Ehrlich's  diazo-reaction  is  of 
little  value  as  it  occurs  both  in  typhoid  fever  and  tuberculosis.  The 
leukocyte  count  is  normal  or  slightly  increased.     Toward  the  end  pul- 


DISEASES    OF   THE    LUNGS  375 

monary  or  meningeal  signs  and  symptoms  or  both  may  be  marked.  In 
the  majority  of  cases,  however,  localizing  signs  are  absent  and  the 
patient  finally  dies  with  all  the  evidences  of  a  general  toxemia. 

Diagnosis. — Considering  the  widespread  distributions  of  the  disease 
and  the  pronounced  character  of  the  symptoms  it  is  remarkable  how  fre- 
quently the  condition  is  mistaken  for  typhoid  fever  or  malignant  endo- 
carditis. It  is  notorious  that  miliary  tuberculosis  is  far  more  often  mis- 
taken for  typhoid  fever  than  the  reverse.  The  confusion  is  greatest  in 
cases  in  which  there  is  no  obvious  tuberculous  focus.  Symptoms  of  ty- 
phoid fever  developing  in  an  individual  with  old  hip-joint  disease  or  other 
chronic  tuberculous  lesion,  should  always  suggest  miliary  tuberculosis. 
In  typhoid  fever  the  temperature  curve  is  characterized  by  a  steady 
ascent  followed  by  a  period  of  slight  remissions  and  later  by  intermissions. 
In  both  miliary  tuberculosis  and  malignant  endocarditis  the  temperature 
is  very  irregular  and  does  not  conform  to  any  definite  type.  Eruptions 
occur  in  all  three  conditions.  That  of  typhoid  fever  consists  of  the 
so-called  "rose  spots"  which  most  often  appear  over  the  abdomen  and 
lower  chest.  A  petechial  eruption  may  be  present  in  both  miliary 
tuberculosis  and  malignant  endocarditis.  This  eruption  may  appear 
on  any  portion  of  the  body  but  in  miliary  tuberculosis  it  shows  a  prefer- 
ence for  the  wrists.  The  presence  of  a  cardiac  murmur  associated  with 
symptoms  of  a  general  toxemia  should  always  suggest  malignant  endo- 
carditis ;  unfortunately  in  not  a  few  of  these  cases  examination  of  the  heart 
gives  no  clue  as  to  the  true  nature  of  the  trouble. 

Modern  laboratory  methods  offer  the  most  certain  means  of  differenti- 
ating these  conditions.  Blood  cultures  will  show  the  presence,  usually  of 
a  streptococcus,  in  cases  of  malignant  endocarditis.  In  typhoid  fever 
Eberth's  bacillus  can  often  be  demonstrated  during  the  early  days  of  the 
disease.  The  Widal  reaction  is  looked  upon  as  strong  evidence  in  favor 
of  typhoid  fever  but  in  several  instances  which  have  come  to  my  notice 
a  positive  Widal  was  obtained  in  cases  which  at  autopsy  proved  to  be 
general  miliary  tuberculosis. 

Pulmonary  Form 

In  this  form  the  brunt  of  the  infection  is  borne  by  the  lungs  and  the 
symptoms  and  physical  signs  are  more  or  less  distinctly  pulmonary  in 
character.  The  onset  may  be  gradual  or  sudden,  usually  the  former. 
In  the  majority  of  instances  when  the  disease  occurs  in  adults  the 
patient  is  known  to  have  a  chronic  pulmonary  lesion  or  to  have  been 
subject  to  a  chronic  cough.  In  children  it  is  most  apt  to  succeed 
one  of  the  acute  infections,  particularly  measles,  or  whooping  cough. 
The  patient  complains  of  malaise,  headache  and  anorexia.  Cough 
and  expectoration  are  always  present.  The  cough  may,  for  a  time, 
be  hacking  in  character  and  unproductive  but  in  most  cases  it  is 
accompanied  by  mucopurulent  expectoration.  The  sputum  is  often 
blood-streaked  and  occasionally  the  presence  of  an  old  cavity  or  more 
or  less  dense  infiltration.  The  signs  of  the  old  lesion  may  consist  of 
nothing  more  than  slight  retraction  and  diminution  of  expansion  and 
suppression  of  the  respiratory  sounds.  Over  the  remainder  of  the  lung 
the  percussion  note  may  be  resonant  or  even  hyperresonant  owing  to 
the  small  size  of  the  miliary  tubercles,  the  fact  that  they  are  scattered 


376      DISEASES   OF   THE  BRONCHI,   LUNGS,   PLEURA,   AND   DIAPHRAGM 

and  also  because  there  are  often  varying  degrees  of  emphysema.  In 
some  instances  patches  of  dulness  may  be  elicited  over  areas  in  which  the 
tubercles  have  coalesced  in  somewhat  the  same  manner  as  occurs  in 
tuberculous  broncho-pneumonia.  In  children  a  broncho-pneumonic 
type  of  the  disease  is  not  unusual.  On  auscultation  the  breath  sounds 
may  be  harsh  but  more  often  they  are  obscured  by  rales.  These  are 
numerous  and  in  the  beginning  are  intense  and  crackling  in  character. 
As  the  disease  progresses  large  mucous  and  sibilant  rales  are  also  heard. 
Over  the  patches  of  consolidation  the  breathing  is  bronchial  or  broncho- 
vesicular  in  character.  The  heart  sounds  may  be  clear  but  often  they 
are  obscured  by  rales.     The  spleen  is  usually  enlarged. 

If  an  old  pulmonary  lesion  is  present  tubercle  bacilli  can  usually  be 
demonstrated  in  the  sputum.  In  the  absence  of  such  a  lesion  tubercle 
bacilli  are  absent  as  death  usually  takes  place  before  the  miliary  tubercles 
break  down.  The  urine  may  show  traces  of  albumen.  The  leukocyte 
count  may  be  normal  or  slightly  increased. 

Diagnosis. — As  has  been  previously  pointed  out  miliary  tuberculosis 
affecting  a  portion  of  the  lung  previously  free  from  disease  is  not  infre- 
quent as  a  terminal  event  in  the  chronic  pulmonary  type  of  tuberculosis. 
As  a  rule  its  presence  is  unrecognized  during  life.  When,  however,  it 
arises  secondarily  to  a  limited  apical  lesion  or  follows  an  attack  of 
measles  or  whooping  cough  in  children  the  diagnosis  is  relatively  easy. 
The  dyspnea,  cyanosis,  cough,  and  evidences  of  a  severe  infection  should 
always  arouse  suspicion.  This  becomes  still  stronger  with  the  finding 
of  evidences  of  pulmonary  damage  at  one  of  the  apices.  The  presence 
of  tubercle  bacilli  in  the  sputum  furnishes  the  positive  proof. 

Meningeal  Form 

(Tuberculous  or  basilar  meningitis,  acute  hydrocephalus,  "water  on 
the  brain.") 

Etiology. — Miliary  tuberculosis  characterized  by  meningeal  symptoms 
is  by  far  the  commonest  form  of  the  disease.  It  occurs  more  often  in 
children  than  adults.  In  100  cases  in  children  collected  by  Still  70  oc- 
curred between  the  second  and  fifth  years.  Tuberculous  meningitis 
is  occasionally  the  terminal  event  in  cases  of  chronic  pulmonary  tubercu- 
losis. The  condition  is  practically  always  secondary  to  a  tuberculous 
lesion  elsewhere  in  the  body.  In  the  few  instances  in  which  it  is  ap- 
parently primary  it  is  probable  that  the  search  for  the  initial  lesion  has 
not  been  sufficiently  thorough.  The  primary  lesion  may  be  located  in 
portions  of  the  body  which  are  omitted  in  a  routine  autopsy,  as  for 
instance,  the  middle  ear  or  the  bones. 

Morbid  Anatomy. — Invasion  of  the  meninges  is  practically  always 
through  the  circulation  being  secondary  therefore  to  a  lesion  elsewhere  in 
the  body.  The  most  common  primary  foci  are  to  be  found  in  the  lungs 
or  lymph  nodes.  Rarely  the  meninges  are  invaded  by  extension  from 
adjacent  structures.  The  tubercle  bacilli  being  deposited  in  the  meninges 
produce  small  tubercles.  These  may  be  few  in  number  and  limited  to 
the  base  of  the  brain  or  they  may  be  quite  widely  scattered.  Often  they 
are  found  along  the  Sylvian  fissure.  The  condition  is  usually  bilateral 
but  one  side  may  be  more  extensively  involved  than  the  other.  The 
tubercles  consist  of  small  whitish  or  grayish-white  nodules  the  size  of  a 


DISEASES    OF    THE    LUNGS  377 

pinhead  or  smaller,  distributed  along  the  course  of  the  blood-vessels. 
In  most  cases  the  tubercles  are  associated  with  a  turbid,  seropurulent 
exudate  which  is  most  marked  at  the  base  of  the  brain.  It  may  extend, 
however,  up  over  the  lateral  hemisphere  of  the  brain  especially  along  the 
Sylvian  fissure.  As  a  result  the  basal  convolutions  may  be  flattened  and 
the  cortex  swollen  and  edematous.  The  pia-arachnoid  is  usually  con- 
gested and  edematous.  The  lateral  ventricles  are  dilated  and  contain 
a  turbid  fluid  similar  to  the  exudation  elsewhere.  Occasionally  the 
process  extends  downward  involving  the  upper  part  of  the  spinal  cord. 

A  chronic  form  is  not  uncommon  in  which  a  single  tuberculous  nodule 
is  formed  as  the  result  of  the  coalescence  of  a  small  cluster  of  tubercles. 
This  type  may  be  more  or  less  latent  or  give  rise  to  symptoms  similar 
to  those  encountered  in  cases  of  brain  tumor. 

Symptoms. — As  the  symptoms  are  dependent  on  irritation  of  the 
nerves  they  will  vary  considerably  in  different  cases  according  to  the 
portion  of  the  central  nervous  system  most  involved.  The  onset  is 
rarely  sudden.  In  children  there  is  apt  to  be  a  history  of  failing  health 
for  a  few  weeks  or  the  child  has  but  recently  recovered  from  an  attack 
of  measles  or  whooping  cough.  In  adults  all  the  cases  of  tuberculous 
meningitis  which  I  have  seen  have  been  associated  with  an  obvious 
primary  lesion,  usually  in  the  lungs;  in  three  instances  there  was  a  tuber- 
culous testicle  also.  The  disease  may  be  ushered  in  suddenly  with  a 
convulsion  but  headache  is  usually  the  first  symptom  which  attracts  at- 
tention. Associated  with  this  symptom,  in  the  majority  of  cases,  are 
vomiting,  constipation  and  fever.  In  children  the  headache  may  manifest 
itself  by  the  child  putting  its  hand  to  its  head  and  if  the  pain  is  severe 
the  child  may  at  the  same  time  cry  or  scream.  The  vomiting  is  often 
explosive  in  character,  occurs  without  apparent  cause  and  is  independent 
of  the  taking  of  food.  The  fever  is  not  marked  in  the  beginning  but 
gradually  becomes  higher.  The  pulse  at  first  rapid  becomes  slow; 
when  present  bradycardia  is  of  great  diagnostic  importance.  Later  the 
abdomen  becomes  retracted  and  symptoms  indicative  of  irritation  of  the 
nerve  centers  appear.  Eye  symptoms  are  common.  These  may  be  pho- 
tophobia, irregularity  of  the  pupils  and  paresis  or  paralysis  of  the  ocular 
muscles.  Facial  paralyses  are  also  seen  at  times  and  Kernig's  sign  can 
often  be  elicited.  In  the  final  stage  there  is  unconsciousness;  retraction 
of  the  head  and  convulsions  may  occur.  The  pulse  again  becomes  rapid 
and  the  temperature  falls  to  normal  or  subnormal. 

In  an  individual  who  is  known  to  be  tuberculous  and  in  whom  there 
develops  severe  headache,  vomiting,  fever,  bradycardia  and  signs  of 
irritation  of  the  nerve  centers,  a  diagnosis  of  tuberculous  meningitis  can 
be  made  with  reasonable  certainty.  In  children  in  whom  it  may  be 
difficult  to  establish  the  presence  of  a  primary  focus,  spinal  puncture 
should  always  be  resorted  to.  The  fluid  withdrawn  is  turbid  and  under 
high  pressure.  The  cellular  elements  are  greatly  increased.  In  the 
very  early  stages  polynuclear  cells  may  predominate  but  later  there  is 
a  marked  lymphocytosis.  In  the  majority  of  cases  tubercle  bacilli  can 
be  demonstrated  in  the  fluid  although  in  some  cases  prolonged  and  patient 
search  is  required. 

The  duration  of  the  -disease  is,  as  a  rule,  from  two  to  four  weeks. 
Occasionally  fulminating  cases  are  seen  in  which  death  takes  place  in  a 
few  days;  in  other  instances  the  disease  is  quite  prolonged  and  chronic. 


378      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,    AND   DIAPHRAGM 

The  accepted  opinion  is  that  tuberculous  meningitis  is  always  fatal  and 
although  several  cases  of  recovery  have  been  reported  many  question  the 
reliability  of  the  observations. 

Mycotic  Infections  of  the  lungs 

The  pulmonary  symptoms  produced  by  mycotic  infections  of  the 
lungs  are,  in  many  instances,  not  to  be  distinguished  from  those  occurring 
in  tuberculosis.  Furthermore,  the  physical  signs  are  apt  to  be  identical 
and  indicate  a  localized  process  at  the  apex,  a  widespread  miliary  process, 
or  a  chronic  type  of  disease  with  consolidation  or  cavity  formation.  In 
view  of  their  great  similarity  to  tuberculosis  in  both  symptoms  and 
physical  signs,  it  is  impossible  to  tell  how  frequent  these  infections  really 
are,  as  those  actually  recorded  in  the  literature  are  comparatively 
few  in  number.  It  is  a  reasonable  assumption,  however,  that  many 
errors  of  diagnosis  do  occur.  It  is  quite  likely  also  that  there  are  not  a 
few  instances  in  which  the  true  nature  of  the  trouble  has  escaped  notice 
even  in  the  autopsy  room,  inasmuch  as  the  small  nodules  could  readily 
be  taken  for  miliary  tubercles.  This  error  could  very  easily  be  made  in 
specimens  of  blastomycosis  of  the  lungs  that  I  have  seen.  In  cases  of 
coccidioidal  granuloma  the  resemblance  is  even  more  pronounced. 

There  are  two  very  common  errors  made  in  determining  the  character 
of  pulmonary  infections.  The  first  is  the  readiness  with  which  many 
practitioners  accept  a  single  negative  sputum  examination  as  evidence 
that  tuberculosis  can  be  ruled  out.  It  must  be  borne  in  mind  that  one  or 
even  a  number  of  negative  examinations  are  of  no  value  in  excluding 
early  tuberculosis,  as  the  great  majority  of  cases  of  true  incipient  tuber- 
culosis do  not  show  tubercle  bacilli  in  the  sputum. 

The  second  error  is  in  assuming  that  because  the  patient  presents 
every  evidence  of  widespread  pulmonary  disease  and  his  symptoms  are 
indicative  of  that  condition  that  there  can  be  no  doubt  of  the  diagnosis. 
It  is  in  cases  of  this  class  that  some  of  the  unusual  types  of  pulmonary 
infection  escape  recognition.  Either  a  sputum  examination  is  not 
considered  worth  while,  or  the  occurrence  of  a  number  of  negative  ex- 
aminations does  not  arouse  the  suspicion  that  some  organism  other  than 
the  tubercle  bacillus,  may  be  the  true  cause  of  the  trouble. 

It  cannot  be  emphasized  too  strongly  that  in  every  case  in  which  the 
symptoms  and  physical  signs  point  to  tuberculosis,  and  yet  repeated 
examinations  of  the  sputum  fail  to  reveal  tubercle  bacilli,  some  other 
infecting  agent  should  be  thought  of. 

PULMONARY  STREPTOTHRICOSIS 

There  is  an  extensive  literature  on  streptothricosis  which  is  more 
or  less  confusing  to  the  student  by  reason  of  the  fact  that  the  disease  has 
been  described  under  such  a  variety  of  names.  The  following  terms  have 
been  employed  to  designate  this  group  of  organisms:  Actinomyces, 
cladothrix,  nocardia,  oospora,  discomyces,  pseudo-tubercle  bacillus,  etc. 
Since  the  appearance  of  the  papers  by  Musgrave,  Clegg,  and  Polk1 
and  Foulerton,2  the  term  streptothrix  adopted  by  these  authorities,  has 

1  Philippine  Jour.  Sc,    190S,   vol.  iii,    447. 

2  Lancet,  Feb.  26;  March  5  and  19,    1910. 


DISEASES    OF    THE    LUNGS  379 

come  into  general  use.  It  is  to  be  understood  that  the  term  is  not  ap- 
plied to  a  single  organism  but  to  a  group  consisting  of  a  number  of  dis- 
tinct species.  While  many  writers  describe  the  actinomyces  as  one  of 
the  species  of  the  streptothrix  group,  it  seems  preferable  to  give  it  a 
separate  place.  This  is  justified  not  only  because  of  certain  distinct 
cultural  differences  but  also  because  of  its  pathological  and  clinical 
manifestations. 

Clinically,  the  streptothrix  group  is  the  most  important  of  the 
mycotic  organisms.  Not  only  is  it  by  far  the  most  common  of  these 
infections  but  in  addition  it  is  readily  confused  with  tuberculosis.  There 
is  good  reason  to  believe  that  streptothricosis  is  much  more  prevalent 
than  the  reported  cases  indicate. 

Etiology. — It  is  not  known  how  the  infection  is  acquired.  Certain 
species  of  the  group  have  a  wide  distribution  in  nature  and  have  been 
found  in  the  air,  water,  soil  and  on  food  stuffs.  It  may  be  assumed  that 
these  organisms,  gain  entrance  into  the  body  in  much  the  same  way  as 
the  tubercle  bacillus  and  that  pulmonary  infection  takes  place,  for  the 
most  part,  by  inhalation  and,  to  a  lesser  extent,  by  ingestion. 

It  is  well  known  that  streptothrix  organisms  can  be  found  in  the 
mouth,  nasopharynx,  crypts  of  the  tonsils  and  in  the  material  from  dental 
caries.  Lord1  has  expressed  the  belief  that  the  tonsils  and  carious  teeth 
are  often  harbingers  for  these  fungi  and  that  they  may  start  up  active 
disease  elsewhere.  Nearly  one-half  of  the  recorded  cases  involve  the 
head  and  neck  regions  (Claypole).  Clinically  this  is  important  as  there 
is  nothing  characteristic  in  the  appearance  of  the  abscesses  or  enlarged 
lymph  nodes  to  differentiate  the  condition  from  tuberculosis.  From  the 
cases  so  far  recorded  it  is  estimated  that  chest  infections  constitute  about 
18  per  cent,  of  all  cases  of  streptothricosis. 

Morbid  Anatomy. — The  distribution  of  the  lesions  in  the  lungs  is 
very  similar  to  that  seen  in  tuberculosis.  The  infection  may  be  limited 
to  the  upper  lobe  or  by  the  time  the  patient  comes  under  observation 
one  lung  and  the  apex  of  the  opposite  lung  may  be  involved.  As  a  rule, 
the  disease  is  slow  and  progressive  and  tends  to  remain  localized  but  it 
may  become  acute  and  assume  a  pneumonic  course.  In  the  final  stage 
the  infected  area  is  markedly  granulomatous,  this  tissue  replacing  all  the 
air  cells  and  bronchioles.  The  nodules  show  little  tendency  to  caseate 
and  break  down  and  cavity  formation  is  unusual.  In  some  instances, 
such  as  the  case  described  by  Flexner,2  small  nodules  resembling  miliary 
tubercles  are  scattered  through  the  lung.  A  marked  feature  of  most 
cases  is  the  formation  of  fibroid  tissue  in  the  lung.  This  doubtless  is 
largely  responsible  for  the  marked  dyspnea  which  is  characteristic  of  the 
trouble  in  many  cases. 

Among  other  pulmonary  lesions  which  have  been  ascribed  to  these 
organisms  may  be  mentioned  broncho-pneumonia,  bronchiectasis,  abscess 
and  gangrene.  The  two  latter  conditions  may  be  the  sequels  to  a  tonsil- 
ectomy,  the  organism  being  squeezed  out  of  the  crypts  and  insufflated 
into  the  air  passages.  In  one  case  seen  at  the  Phipps  Institute  the  only 
explanation  of  an  extensive  unilateral  pulmonary  fibrosis  seemed  to  be 
a  streptothrix  organism.  In  several  other  instances  in  which  the  fibrosis 
was  associated  with  bronchiectasis,  streptothrix  organisms  were  found 

1  Jour.  Am.  Med.  Assoc,  1910,   lx,  p.  1261. 

2  Trans.  Assoc.  Am.  Phys.,  1898,    p.  31. 


380      DISEASES   OF  THE  BRONCHI,   LUNGS,   PLEURA,   AND  DIAPHRAGM 

among  an  extensive  bacterial  flora;  but  in  these  cases  it  was  not  possible 
to  determine  whether  the  streptothrix  organism  was  a  primary  or  a 
secondary  invader.  Fibrinous  pleurisy  and  empyema  occasionally 
occur.  Perforation  of  the  chest  wall  is  rare  in  marked  contrast  to  the 
frequency  with  which  this  accident  occurs  in  cases  of  infection  with  the 
actinomyces. 

Metastatic  lesions  are  not  uncommon,  especially  in  the  brain. 

Symptoms. — The  extraordinary  fidelity  with  which  infection  with  this 
group  of  organisms  may  ape  pulmonary  tuberculosis  is  gradually  becom- 
ing more  and  more  apparent.  Bridge1  has  reported  17  cases,  in  12  of 
which  the  persistent  absence  of  tubercle  bacilli  was  the  only  evidence 
against  the  diagnosis  of  tuberculosis.  The  symptoms  and  physical  signs 
were  identical  with  those  encountered  in  the  latter  disease.  In  5  cases 
both  streptothrix  organisms  and  tubercle  bacilli  were  found.  Recently 
Stockwell2  has  made  a  most  important  contribution  to  this  subject. 
Among  some  600  patients  admitted  to  the  sanatorium  of  which  he  had 
charge  he  found  12  patients  in  whom  the  symptoms  and  physical  signs 
were  essentially  those  of  tuberculosis.  Tubercle  bacilli  were  persistently 
absent  and  in  each  case  a  streptothrix  organism  was  found. 

Stockwell  emphasizes  the  fact  that  the  general  condition  of  patients 
suffering  from  pulmonary  streptothricosis  is  notably  good  and  that  they 
do  not  give  the  impression  of  being  ill.  This  fact  is  especially  note- 
worthy when  the  amount  of  pulmonary  damage  is  taken  into  account. 
In  two  instances  the  appearance  of  good  health  was  maintained  until 
shortly  before  death. 

In  common  with  tuberculosis  cough,  mucopurulent  sputum,  fever 
and  some  acceleration  of  the  pulse  rate  are  present  in  all  cases.  Loss  of 
weight  occurs  in  most  cases  and  may,  in  some  instances,  be  marked. 

Dyspnea  which  is  not  an  especially  important  symptom  in  tuberculosis 
is  very  common  in  streptothricosis  and  may  be  the  one  symptom  for 
which  the  patient  seeks  relief.  This  is  probably  due  to  the  extensive 
fibroid  changes  which  occur  in  the  lungs.  In  some  instances  the  sputum 
is  foul-smelling  as  the  result  of  an  associated  bronchiectasis.  A  frank 
hemoptysis  or  the  more  or  less  constant  presence  of  blood-streaked 
sputum  is  a  common  symptom.  Chest  pain  or  the  occurrence  of  a 
definite  pleurisy  is  also  encountered  in  a  large  proportion  of  the  cases. 

Physical  Signs. — There  is  nothing  characteristic  about  the  physical 
signs.  As  a  rule,  the  disease  is  found  in  one  of  the  upper  lobes  or  when  the 
patient  is  first  seen  all  of  one  lung  and  the  upper  lobe  on  the  opposite  side 
may  be  diseased.  The  signs  are  those  obtained  in  any  infiltrating  process, 
namely,  restriction  of  motion,  impairment  of  the  percussion  note,  broncho- 
vesicular  breathing,  which  is  often  more  or  less  suppressed,  and  exaggerated 
voice  sounds  and  rales.  Less  commonly  there  may  be  cavity  signs. 
Occasionally  one  or  both  bases  of  the  lungs  are  diseased  while  the  upper 
lobes  are  healthy;  these  should  not  be  confused  with  tuberculosis. 

It  can  readily  be  seen  that  so  far  as  the  symptoms  and  physical  signs 
are  concerned  a  correct  diagnosis  is  not  possible  without  a  sputum  ex- 
amination. If  tubercle  bacilli  are  persistently  absent  from  the  sputum 
of  patients  who  present  every  other  evidence  of  tuberculosis,  a  diagnosis 
of  the  latter  condition  is  not  tenable.     Under  these  circumstances  the 

T-Jour.  Am.  Med.   Assoc,  1911,  vol.  ii,  p.  1501. 

2  Trans.  Nat.  Assoc,  for  the  Study  and  Prevention  of  Tuberculosis,    1916. 


DISEASES    OF    THE    LUNGS  381 

sputum  should  be  examined  for  the  presence  of  one  of  the  mycotic 
organisms. 

Sputum  Examination. — A  24-hour  specimen  should  be  searched  for 
small  yellowish  granules  about  the  size  of  a  pinhead.  These  will  be 
found  in  the  purulent  and  not  the  watery  portion  of  the  sputum.  These 
small  granules  should  be  stained  with  carbol-fuchsin  and  Gram  stains. 
The  stained  specimen  shows  the  organism  as  isolated,  slender  filaments 
or  a  loose  network  of  filaments  which  may  be  stained  uniformly  or 
present  a  beaded  appearance.  The  staining  properties  of  this  group 
vary  considerably  especially  with  reference  to  acid  fastness;  some  are 
readily  decolorized;  others  are  moderately  acid-fast;  and  still  others  are 
almost  as  resistant  to  acid  as  the  tubercle  bacillus.  This  is  important 
to  bear  in  mind  as  one  who  is  possessed  of  but  a  superficial  knowledge  of 
bacteriology  may  readily  mistake  some  of  the  short  fragments  for  tubercle 
bacilli.  This  mistake  may  occur  if  Gabbet's  stain  is  employed  as  the 
decolorizing  agent.  An  instance  of  this  has  come  to  my  notice  and  in 
one  of  Bridge's1  cases  a  similar  mistake  apparently  occurred.  Strepto- 
thrix  organisms  are  readily  decolorized  with  30  per  cent,  nitric  acid.  If 
the  tonsils  contain  cheesy  crypts,  or  dental  caries  is  present,  these  sources 
of  contamination  should  be  eliminated. 

Cutaneous  Test. — Claypole2  has  differentiated  a  number  of  species  and 
from  glycerinated  bouillon  cultures  prepared  streptotrichins.  She  found 
that  skin  tests  made  in  the  same  manner  in  which  tuberculin  is  em- 
ployed gave  definite  reactions  in  people  with  frank  streptothrix  infec- 
tions. Both  tuberculosis  and  streptothricosis  may  occur  in  the  same 
individual. 

Diagnosis. — This  rests  on  the  finding  of  the  streptothrix  in  the 
sputum.  If  possible  the  skin  tests  should  be  employed  also.  Institu- 
tions dealing  with  tuberculosis  should  make  it  a  fixed  rule  to  examine  the 
sputum  for  one  of  the  mycotic  organisms  in  all  patients  having  the 
symptoms  and  physical  signs  of  tuberculosis  but  in  whom  tubercle  bacilli 
are  absent.  If  this  procedure  be  carried  out  routinely  it  is  highly  prob- 
able that  the  percentage  of  cases  of  streptothricosis  will  be  greatly  in- 
creased. For  the  welfare  of  the  patient  a  correct  diagnosis  is  highly 
important,  as  the  use  of  iodide  of  potassium  in  cases  of  streptothricosis 
is  often  followed  by  splendid  results. 

PULMONARY  ACTINOMYCOSIS 

Etiology. — In  certain  parts  of  the  world  infection  with  the  actinomyces 
is  fairly  frequent,  namely,  Germany,  Russia  and  Austria.  In  the 
London  hospitals3  no  less  than  135  instances  of  the  disease  were  en- 
countered in  the  decade  of  1902  to  1912.  In  this  country,  although 
isolated  case  reports  appear  from  time  to  time,  the  disease  may  be  said 
to  be  comparatively  rare  in  man. 

The  disease  is  widespread  among  cattle,  and  is  often  referred  to  as 
"big-jaw."  It  is  occasionally  met  with  in  other  domestic  animals. 
There  is  no  evidence,  however,  that  infection  in  man  is  acquired  either 
from  the  milk  or  meat  of  diseased  cattle,  and  it  is  exceptional  that  infec- 

1  Loc.  cit. 

2  Trans.  Nat.  Assoc,  for  the  Study  awl  Prevention  of  Tuberculosis,  1914. 
3Proc.  Royal  Sor.  Med.,  1912-1913. 


382      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

tion  occurs  in  man  from  direct  contact  with  a  diseased  animal.  The 
infection  is  believed  to  be  acquired  in  the  majority  of  instances  by  those 
engaged  in  the  handling  of  straw  and  grain,  and  by  those  in  close  contact 
with  vegetable  products.  Infection  apparently  is  through  the  alimentary 
or  respiratory  tracts,  as  it  is  in  direct  connection  with  these  that  the 
disease  is  usually  encountered. 

Statistical  studies  which  have  been  made  indicate  that  the  infection 
is  primarily  a  pulmonary  one  in  from  15  to  18  per  cent,  of  the  reported 
cases. 

Morbid  Anatomy. — Actinomycosis  may  manifest  itself  as  a  diffuse 
bronchitis;  a  widespread  miliary  process,  or  as  a  result  of  coalescence  of 
the  actinomycotic  nodules,  necrosis  and  cavity  formation  may  occur. 

The  disease  may  involve  either  one  or  both  lungs.  The  initial  infec- 
tion is  believed  by  some  to  occur  more  frequently  in  one  of  the  lower 
lobes,  although  in  most  instances  the  disease  has  become  so  widespread 
by  the  time  it  is  recognized  that  the  primary  focus  cannot  be  determined. 

The  changes  produced  in  the  lungs  consist  of  the  formation  of  small 
nodules  not  unlike  tubercles.  These  nodules  may  coalesce  forming 
masses  of  considerable  size  and  resembling  sarcoma.  As  the  disease 
progresses,  an  area  of  necrosed  cells  appear  about  the  nodules  and  about 
this  area  a  round-celled  proliferation  occurs.  Connective-tissue  pro- 
liferation is  usually  marked  about  the  nodules.  The  tendency  of  the 
disease  seems  to  be  to  spread  by  direct  continuity  of  tissue  and,  unlike 
tuberculosis,  to  ignore  anatomical  boundaries,  and  cause  adhesions  by 
involving  all  and  every  structure  with  which  it  comes  into  contact; 
in  this  respect  it  resembles  malignant  disease. 

When  the  lung  is  the  seat  of  the  primary  infection  the  pulmonary  focus 
will  spread  by  continuity  of  tissue  until  it  has  reached  the  pleural  surface. 
The  two  surfaces  of  the  pleural  sac  then  become  adherent,  the  disease 
spreading  across  the  adherent  surfaces  and  finally  rupturing  through  an 
intercostal  space  without  the  occurrence  of  an  empyema,  although  the 
latter  is  commonly  believed  to  be  the  real  source  of  the  trouble.  The 
abscess  may  occur  at  almost  any  part  of  the  chest  wall.  In  like  manner 
any  or  all  of  the  thoracic  contents  may  be  involved  by  the  disease. 

When  the  lung  is  the  primary  seat  of  the  disease,  the  cutaneous  lesion 
occurs  somewhere  on  the  chest  wall.  It  is  to  be  borne  in  mind,  however, 
that  pulmonary  disease  may  be  secondary  to  a  lesion  in  other  parts  of 
the  body.  More  than  half  of  the  recorded  cases  show  that  the  primary 
lesion  involves  the  skin  of  the  face  and  neck;  it  may  appear  also  in  the 
structures  within  the  mouth. 

The  cutaneous  lesion  is  characteristic  in  appearance.  The  skin  itself 
is  apparently  infected  only  in  a  slight  degree,  except  that  it  is  punctuated 
here  and  there  by  small  ulcers  which  mark  the  sites  of  discharge  of  small 
abscesses  in  the  subcutaneous  tissue.  The  surrounding  skin  is  apt  to 
present  a  dusky  appearance  because  of  the  changes  in  the  underlying 
subcutaneous  tissue,  and  there  is  rarely  any  spreading  of  the  ulceration. 
Perhaps  the  most  noticeable  feature  of  the  lesion  is  the  curious  linear 
puckering  which  occurs  in  the  area  about  the  ulcer. 

Symptoms. — In  pulmonary  actinomycosis  the  onset  is  gradual,  the 
patient  complaining  of  weakness  and  gradual  loss  of  strength  and 
weight.  Sooner  or  later  cough  and  expectoration  develop.  The  latter 
is  commonly  mucopurulent  in  character  and  in  many  of  the  cases  the 


DISEASES    OF    THE    LUNGS  383 

small  sulphur  granules  which  are  characteristic  of  the  disease  may  be 
seen.  Blood-streaked  sputum  and  hemorrhage  are  of  infrequent  occur- 
rence. The  fever  is  irregular  or  hectic  in  type.  With  involvement  of 
the  pleura,  pain  is  experienced,  and  this  may  be  dull  or  aching  in  character 
or  sharp  and  stabbing  as  in  acute  pleurisy. 

As  the  disease  progresses  the  chest  wall  becomes  involved  and  later 
an  abscess  appears  in  one  of  the  intercostal  spaces.  Because  of  the  pain, 
the  physical  signs  and  the  discharge  of  pus  through  an  interspace,  an 
empyema  or  caries  of  a  rib  is  usually  thought  to  be  present. 

Physical  Signs. — A  thorough  inspection  is  essential  because  of  the 
associated  cutaneous  lesion,  the  recognition  of  which  is  of  the  greatest 
aid  in  making  a  correct  diagnosis. 

Neither  the'  percussion  nor  the  auscultatory  findings  give  any  clue 
as  to  the  true  nature  of  the  trouble. 

The  following  case  is  a  typical  example  of  primary  pulmonary 
actinomycosis  observed  in  the  Phipps  Institute  several  years  ago. 

Case  No.  5376.  Male,  aged  ten.  Family  history,  negative.  Child  was  said  to 
have  had  pneumonia  followed  by  empyema  which  was  drained  when  three  years  of 
age.     Ill  health  ever  since. 

Symptoms. — Cough,  yellowish-white  expectoration,  one  hemoptysis,  dyspnea  and 
some  chest  pain.  Patient  died  four  weeks  after  admission  to  the  hospital.  During 
this  period  he  had  a  high  continuous  type  of  temperature  (103°F.)  withs  light  daily 
remissions,  very  rapid  heart  action  and  extreme  dyspnea.  Five  sputum  examinations 
were  negative  for  tubercle  bacilli. 

Physical  Signs. — The  patient  presented  an  emaciated  appearance  with  restriction 
of  motion  over  both  upper  lobes.  Marked  dulness  over  both  upper  lobes  and  at  right 
base  (site  of  old  empyema).  Over  the  dull  area  the  breathing  was  either  bronchial  or 
broncho-vesicular  in  character  with  many  crepitant  and  medium-sized  rales. 

Both  the  symptoms  and  physical  signs  pointed  to  advanced  pulmonary  tuber- 
culosis. The  warning  of  five  negative  sputum  examinations  was  not  heeded.  After 
the  diagnosis  of  actinomycosis  had  been  made  at  the  autopsy  a  specimen  of  sputum, 
sent  to  the  laboratory  the  day  before  the  child's  death,  was  examined  and  showed 
both  the  sulphur-like  granules  macroscopically  and  the  stained  organism  microscop- 
ically. 

Autopsy  Findings. — Left  lung,  upper  lobe  grayish-yellow  in  color  on  section  granu- 
lar and  markedly  edematous  with  scattered  nodules  size  of  pinhead  resembling  an 
early  stage  of  tubercle.  Throughout  the  lower  lobe  are  numerous  shallow  cavities 
filled  with  small  bodies  of  the  size  and  color  of  actinomycotic  granules. 

The  bronchi  contains  granular  material. 

Right  lung  was  firmly  bound  down  by  dense  pleuritic  adhesions.  The  upper  lobe 
was  yellowish  in  color  and  showed  early  gangrenous  changes.  On  section  dirty 
grayish-yellow  pus  exuded.  The  middle  lobe  contained  several  shallow  cavities  on 
the  external  surface  containing  granular  material  resembling  actinomycotic  granules. 

The  lower  lobe  showed  no  evidence  of  empyema.  There  were  some  isolated 
bodies  resembling  early  tubercles. 

The  bronchial  glands  were  enlarged  and  caseous.  Histologically  sections  from  the 
lungs  showed  edema,  areas  of  broncho-pneumonia  and  rounded  bodies  having  the 
appearance  of  actinomycotic  granules.  The  tissue  about  these  granules  was  necrotic 
and  beyond  the  necrotic  areas  there  was  cellular  infiltration.  There  was  no  evidence 
of  tuberculosis. 

Diagnosis. — Pulmonary  actinomycosis  is  to  be  distinguished  from 
tuberculosis,  chronic  bronchitis,  empyema  and  caries  of  a  rib.  Unless 
the  lesion  is  localized  at  the  base  of  the  lung  the  physical  signs  taken  in 
conjunction  with  the  symptoms  will  almost  certainly  lead  to  a  diagnosis 
of  tuberculosis,  providing  the  warning  of  the  absence  of  tubercle  bacilli 
in  the  sputum  is  not  heeded.  Macroscopic  examination  of  the  sputum 
f  requently  shows  the  presence  of  the  sulphur  granules,  but  in  their  absence 


384       DISEASES    OF   THE   BROXCHI,    LUNGS,    PLEURA,    AXD   DIAPHRAGM 

the  sputum  should  be  examined  microscopically  for  the  streptothrix 
actinomyces. 

Chronic  bronchitis  is  usually  a  secondary  condition.  If  there  is  no 
associated  lesion  to  account  for  it,  and  the  sputum  is  negative  for  tubercle 
bacilli,  a  mycotic  infection  should  be  considered. 

When  the  lesion  is  localized  at  the  base  of  the  lung,  and  in  addition 
pleuritic  pain  is  present  and  a  discharge  of  pus  occurs  through  an  inter- 
space the  presence  of  an  empyema  is  usually  suspected.  Before  making 
a  diagnosis  of  empyema  one  should  be  certain  that  there  is  no  displace- 
ment of  the  viscera,  such  as  occurs  with  free  fluid  within  the  pleural 
cavity.  An  exploratory  puncture  for  fluid  should  also  be  done.  If 
the  case  be  one  of  actinomycosis,  no  pus  will  be  obtained  or  only  a  very 
slight  amount  if  a  small  superficial  cavity  is  reached.  Sulphur  granules 
may  be  noted  in  the  pus.  An  X-ray  examination  is  of  service  also  in 
differentiating  between  pus  and  pulmonary  consolidation. 

A  mistaken  diagnosis  of  simple  caries  of  a  rib  will  be  avoided  by  noting 
the  character  of  the  cutaneous  change  and  the  associated  pulmonary 
signs. 

In  any  case  the  final  diagnosis  rests  upon  the  finding  of  the  streptothrix 
actinomyces. 

PULMONARY  BLASTOMYCOSIS 

Etiology. — The  predisposing  causes  of  this  infection  are  not  known. 
A  fact  worthy  of  notice  is  that  the  majority  of  the  cases  reported  in  this 
country  have  occurred  in,  or  in  the  immediate  vicinity  of,  Chicago. 
The  original  source  of  the  infection  is  not  altogether  clear.  Stober1 
has  called  attention  to  the  fact  that  a  number  of  the  patients  have  lived 
in  insanitary  dwellings  in  which  molds  are  readily  demonstrable  on  the 
damp  and  decaying  woodwork.  This  suggests  the  possibility  that  the 
molds  which  infect  man  may  also  have  their  habitat  in  these  insanitary 
surroundings.  In  addition  it  is  the  present  belief  that  in  systemic  blasto- 
mycosis, infection  through  the  respiratory  tract  is  the  most  common  point 
of  entrance.  Even  in  those  cases  in  which  a  cutaneous  lesion  is  ap- 
parently the  only  evidence  of  the  disease  the  original  focus  may  be  an 
unrecognized  pulmonary  lesion. 

Morbid  Anatomy. — When  the  disease  attacks  the  respiratory  tract 
the  bronchi  are  first  involved  with  the  development  of  broncho-pneu- 
monic areas  in  the  neighborhood.  The  disease  may  spread  through  the 
lung  by  way  of  the  bronchi  or  through  the  blood  stream;  in  the  latter 
case  metastases  occur  in  other  parts  of  the  body.  The  pericardium, 
pleura  and  mediastinum  may  become  involved  through  the  lymph 
channels. 

The  disease  majT  be  and  often  is  limited  to  the  upper  lobes,  the  right 
side  being  involved  much  oftener  than  the  left.  The  infiltration  may  be 
slight  and  involve  but  a  slight  area;  it  may  be  widely  scattered  as  in 
miliary  tuberculosis,  and  in  severe  cases  complete  consolidation  of  the 
lung  may  result.  The  nodules  may  be  discrete  without  anjT  associated 
inflammatory  changes,  or  they  may  become  confluent,  forming  larger 
areas  with  a  necrotic  center,  which  may  break  down.  In  the  more  chronic 
types  there  may  be  extensive  fibroid  changes  and  dilatation  of  the 
bronchi. 

1  Arch.  Int.  Med..  April,  1914. 


DISEASES    OF    THE    LUNGS 


385 


The  skin  lesions  may  appear  in  the  form  of  subcutaneous  abscesses 
or  pustules ;  the  latter  are  usually  multiple  and  may  occur  successively 
or  in  crops.  The  lesion  may  primarily  take  the  form  of  an  ulcer,  or  the 
ulcer  may  develop  in  the  site  of  a  ruptured  abscess.  The  ulcer  is  "  usually 
surrounded  by  an  areola  of  inflammation;  the  margins  are  raised  and 
irregular,  and  the  base  is  soft  and  covered  with  granulation  tissue,  which 
may  become  fungoid  and  approach  the  surface,  later  assuming  a  papillo- 
matous appearance,  which  is  more  or  less  characteristic  of  the  lesions  of 
chronic  blastomycosis  of  the  skin"  (Fig.  270).  Furthermore,  as  the 
lesion  spreads  peripherally  it  tends  to  heal  in  the  center. 


Fig.  270. — A  typical  lesion  of  cutaneous  blastomycosis,  c,  Papillomatous  or  ver- 
rucose  surface;  m,  raised  indurated  border  containing  miliary  abscesses;  sc,  scar  of  old 
lesion.      (By  Courtesy  of  Dr.  O.  S.  Ormsby.) 

Symptoms. — In  systemic  blastomycosis  the  initial  symptoms  may 
be  hardly  noticeable;  more  commonly  they  are  those  of  an  acute  infec- 
tion of  the  respiratory  tract.  This  may  resemble  an  ordinary  "cold;" 
in  the  severer  cases  there  is  pain  in  the  chest,  fever,  dyspnea,  cough  and 
the  expectoration  of  blood-streaked  mucopurulent  material.  Sooner  or 
later  the  cutaneous  lesions  appear. 

As  the  disease  progresses  there  is  a  gradual  loss  of  weight  and  strength, 
accompanied  with  malaise,  fever,  irregular  in  character,  but  usually 
showing  an  afternoon  rise ;  cough  is  usually  present,  and  often  severe  in 
character.  The  sputum  is  purulent  or  mucopurulent  and  often  blood- 
streaked.  Occasionally  a  frank  hemorrhage  occurs.  Owing  to  the 
pleural  involvement,  chest  pain  is  common  either  in  the  form  of  a  dull 
aching  sensation,  or  occasionally  a  sharp  stabbing  pain. 

25 


386      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

In  the  terminal  stages  of  the  disease  emaciation  may  be  very  marked. 
At  times,  however,  the  pulmonary  lesions  are  found  post-mortem  to  be 
far  more  extensive  than  either  the  symptoms  or  physical  signs  indicated. 
This  is  probably  clue  to  the  fact  that  in  some  cases  there  is  little  or  no 
inflammatory  reaction  about  the  blastomycotic  nodules. 


Fig.  271. — Right  lung,  Case  23.  ca,  Bronchiectatic  cavity  in  the  fibroid  upper  lobe; 
ab,  abscesses  whose  contents  were  inspissated  and  surrounded  by  a  wall  of  connective 
tissue;  no,  blastomycotic  nodules  in  the  lower  lobe,  which  from  their  distribution  seem  to 
be  bronchogenic  in  origin;  pi,  thickened  pleura.      (Boughton  and  Clark.) 

Physical  Signs. — A  thorough  inspection  is  of  the  utmost  importance. 
This  may  reveal  the  presence  of  a  swollen  and  painful  joint,  or  a  cutaneous 
lesion. 

Restriction  of  expansion,  flattening  and  other  signs  indicative  of 
pulmonary  damage  are  not  peculiar  to  this  disease.     And  the  same  is  to 


DISEASES    OF    THE    LUNGS  387 

be  said  of  the  percussion  and  auscultatory  findings  which  are  usually 
identical  with  those  encountered  in  pulmonary  tuberculosis. 

The  following  case  was  seen  at  the  Phipps  Institute  during  the  past 
year.  Case  No.  14912.  A  young  Indian  girl,  aged  eighteen,  was  referred 
to  the  wards  of  the  Institute  as  a  case  of  tuberculosis.  She  had  com- 
plained of  feeling  badly  for  nearly  a  year.  Six  weeks  prior  to  her  ad- 
mission she  developed  a  cough  and  slight  expectoration,  mucopurulent  in 
character.  She  had  lost  weight  and  had  a  slight  rise  in  temperature  every 
afternoon.     She  was  also  subject  to  paroxysmal  attacks  of  dyspnea. 

Physical  examination  showed  nothing  abnormal  in  the  upper  part  of 
the  lungs.  Over  both  bases  there  was  restricted  motion,  dulness  on  per- 
cussion, and  feeble  breath  sounds  and  fine  rales.  Near  the  angle  of  the 
left  scapula  there  were  marked  pectoriloquy  and  bronchial  breathing. 
X-ray  examination  confirmed  the  clinical  findings  (see  Fig.  353).  Owing 
to  the  location  of  the  lesions  and  the  absence  of  tubercle  bacilli  the  sputum 
was  more  thoroughly  studied  by  my  colleague,  Paul  A.  Lewis.  He  found 
that  the  sputum  contained  the  blastomycotic  organism  in  pure  culture 
and  that  other  tests  confirmed  this  finding. 

Diagnosis. — Both  the  symptomatology  and  the  physical  signs  of 
pulmonary  or  systemic  blastomycosis  often  resemble  tuberculosis  so 
closely  that  a  differentiation  between  the  two  is  impossible  without  a 
sputum  examination.  Fig.  271  illustrates  how  easily  a  mistaken  diag- 
nosis of  tuberculosis  could  be  made. 

As  we  have  pointed  out  already,  given  a  case  which  does  not  show 
tubercle  bacilli,  after  a  number  of  examinations,  some  other  cause  of  the 
trouble  must  be  sought  for. 

COCCIDIOIDAL  GRANULOMA  (California  Disease) 

Until  within  the  past  few  years  this  disease  was  confused  with  blasto- 
mycosis. Recent  studies,  among  which  may  be  mentioned  those  of 
MacNeal  and  Taylor1  and  Brown  and  Cummins2  have  shown  clearly 
that  although  the  two  diseases  resemble  each  other,  a  differentiation  may 
be  made  both  from  the  clinical  picture  and  the  morphological  and 
cultural  characteristics  of  the  infecting  organisms. 

Etiology. — The  cause  of  coccidioidal  granuloma  is  the  coccidioides 
immitis,  the  true  nature  of  which  was  first  discovered  by  Ophuls  and  later 
by  Wolbach.  Prior  to  this  it  was  thought  the  disease  was  due  to  a 
protozoon.  These  observers  showed  that  the  infecting  organism  belonged 
to  the  yeast  group  and  was  closely  related  to  the  blastomyces.  The  two 
organisms  are  differentiable  by  the  endo-sporulation  in  the  coccidioides 
and  the  budding  in  the  blastomyces. 

With  but  two  or  three  exceptions  all  of  the  cases  of  Coccidioidal  granu- 
loma so  far  reported,  have  occurred  in  the  San  Joaquin  Valley,  California. 
Inasmuch  as  there  is  no  evidence  of  direct  association  of  one  case  with 
a  preexisting  case  the  presumption  is  strong  that  there  must  be  some 
important  local  factor  in  causation.  Recently  Lipsitz,  Lawson  and 
Fessenden3  have  reported  the  case  of  a  negro  who  lived  in  Missouri  and 
had  never  been  in  California.     Most  of  the  patients  have  belonged  to 

1  Jour.  Med.  Res.,  July,  1914. 

2  Arch.  Int.  Med.,  April,  1915. 

3  Jour.  Am.  Med.  Assoc.,  April  29,  1916. 


388      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

the  class  of  day  laborers.  So  far  but  one  female  has  been  reported  as 
suffering  from  the  disease. 

Since  the  disease  was  first  described  twenty-one  years  ago  about 
40  cases  have  been  recognized.1  Of  recent  years  the  number  of  cases 
has  increased.  This  is  probably  due  to  the  fact  that  physicians  are 
becoming  more  familiar  with  the  disease. 

Morbid  Anatomy. — The  initial  lesion  may  occur  in  the  skin  of  the 
hands  or  feet,  especially  the  former.  If  seen  in  its  early  stages  the 
initial  lesion  takes  the  form  of  a  papule  or  nodule  which  tends  to  form  an 
ulcer  very  quickly.  It  is  in  the  ulcerated  state  that  the  lesion  is  usually 
first  seen.  The  appearance  of  the  ulcer  has  been  compared  to  a  variety 
of  conditions.  MacNeal  and  Taylor  state  that  the  ulcers  sometimes 
resemble  mycosis  fungoides.  P.  K.  Brown2  has  likened  them  to  the 
crusty  lesions  of  pellagra;  later  they  break  down  and  resemble  syphilitic 
or  tuberculous  ulcers.  In  place  of  the  skin  lesions  painless  subcutaneous 
abscesses  are  sometimes  seen.  The  disease  may  also  attack  the  bones, 
producing  caries,  or  involve  the  joints  giving  rise  to  a  form  of  arthritis 
which  may  be  mistaken  for  tuberculosis.  Meningitis  due  to  the 
coccidioides  has  been  noted  also. 

In  most  instances  the  primary  infection  is  in  the  lungs  although  later 
skin  ulcers  or  subcutaneous  abscesses  may  form.  In  the  lungs  the 
lesions  are  those  of  a  disseminated  miliary  tuberculosis.  The  nodules 
are  grayish  in  color  and  in  places  coalesce.  Small  cavities  are  sometimes 
formed.  Grossly  the  nodules  cannot  be  distinguished  from  tubercles. 
Hektoen3  states:  "This  disease  presents  the  best  mimicry  of  tuberculosis 
ever  seen  and  the  lesions  cannot  be  distinguished  from  tubercles  by  the 
microscopic  anatomy." 

An  excess  of  fluid  in  the  pleural  cavity  is  occasionally  present.  Cocci- 
dioidal disease  differs  from  blastomycosis  in  that  it  shows  a  greater 
predilection  for  the  lymphatic  system,  the  skin  lesions  show  a  greater 
tendency  to  ulcerate,  and  in  systemic  cases  recovery  is  unknown. 

Symptoms. — It  is  emphasized  by  all  who  have  had  experience  with 
coccidioidal  granuloma  that  the  symptoms,  the  clinical  course  and  the 
pathological  picture  is  often  indistinguishable  from  tuberculosis. 

As  already  stated  the  initial  manifestation  may  be  a  skin  lesion,  a 
painless  subcutaneous  abscess,  or  an  arthritis.  Whether  the  lungs  are 
involved  primarily  or  secondarily,  the  symptoms  and  course  of  the  dis- 
ease differ  in  no  particular  from  those  occurring  in  tuberculosis.  The 
patient  loses  weight,  tires  easily,  has  a  cough,  mucopurulent  sputum, 
which  is  often  blood-streaked,  and  afternoon  fever.  As  the  disease 
progresses  the  patient  suffers  from  night  sweats,  emaciates  and  becomes 
anemic.  Rarely  the  disease  remains  localized  but  early  involvement  of 
the  regional  lymph  nodes  and  dissemination  is  the  general  rule.  Occa- 
sionally the  fever  is  high  and  continuous  and  the  disease  pursues  a  very 
rapid  course  not  unlike  that  seen  in  cases  of  tuberculous  broncho-pneu- 
monia. A  very  high  leukocyte  count  may  be  present,  a  point  of  some 
importance  as  a  low  leukocyte  count  or  even  a  leukopenia  is  the  rule  in 
tuberculosis. 

The  disease  is  almost  invariably  fatal.     But  three  cases  have  been 

1  Dickson:  Arch.  Int.  Med.,  December,  1915. 

2  Trans.  Amer.  Climat.  and  Clin.  Assoc,  1915. 

3  Jour.  Am.  Med.  Assoc,  1907,  xlix,  1071. 


DISEASES    OF   THE    LUNGS  389 

known  to  recover.     If  the  process  becomes  localized  in  a  joint,  amputation 
or  resection  may  prevent  dissemination. 

Physical  Signs. — These  differ  in  no  respect  from  what  one  finds  in 
cases  in  which  the  pulmonary  infiltration  is  due  to  tubercles. 

PULMONARY  ASPERGILLOSIS 

Etiology. — A  rare  form  of  mould  infection  is  that  known  as  aspergillosis, 
the  exciting  cause,  in  most  instances,  being  the  aspergillus  fumigatus. 
A  monograph  by  Renon1  is  the  most  authoritative  study  yet  made  of 
this  disease.  Most  of  the  reported  cases,  both  in  man  and  in  animals, 
have  occurred  in  France.  The  occupation  of  the  individual  is  of  some 
importance  as  it  has  been  observed  chiefly  in  those  who  handle  grain, 
flour  or  meal.  Men  engaged  in  the  forcible  feeding  (mouth  to  beak) 
of  pigeons,  and  hair-combers,  who  use  flour  to  remove  the  grease  from  the 
hair,  have  also  acquired  the  disease. 

The  disease  is  extremely  rare  in  this  country.  Osier  has  reported  a 
case  in  which  the  mycelium  and  spores  of  the  aspergillus  were  present 
in  the  sputum  at  intervals  for  a  period  of  twelve  years.  The  patient 
was  in  good  health  having  no  symptoms  other  than  cough  and  slight 
expectoration.  In  Holden's2  case  there  was  involvement  of  the  lungs 
and  the  cervical  and  axillary  lymph  nodes.  In  this  case  the  organism 
was  identified  as  the  aspergillus  nidulans. 

Morbid  Anatomy. — The  apices  of  the  lung  are  apt  to  be  most  involved. 
The  pulmonary  lesions  occur  in  the  form  of  nodules,  from  2  to  4  cm.  in 
diameter,  which  project  from  the  cut  surface.  Emphysema  may  be 
present  about  the  nodules.  In  the  latent  type  of  the  disease  considerable 
fibrosis  occurs  with  dilatation  of  the  bronchi.  The  walls  of  the  dilated 
bronchi  contain  small  white  or  yellowish-white  bodies  which  consist  of 
mycelial  threads.     These  bodies  may  appear  in  the  sputum. 

Aspergillosis  may  occur  also  in  the  lymph  nodes  and  as  a  secondary 
infection  in  chronic  bronchitis,  bronchiectasis  or  pulmonary  tuberculosis 
Under  these  circumstances  its  presence  would  not  be  suspected  unless 
the  sputum  were  especially  examined. 

Symptoms. — There  is  nothing  distinctive  in  the  symptomatology  of 
the  disease.  The  onset  is  as  a  rule  gradual  with  malaise,  loss  of  strength 
and  weight,  anorexia,  a  slight  evening  rise  in  the  temperature  and  pleuritic 
pains.  The  cough  is  at  first  dry  and  unproductive,  but  is  soon  attended 
with  a  frothy  expectoration  which  later  becomes  greenish  and  purulent. 
The  sputum  is  often  blood-tinged  and  the  first  intimation  of  pulmonary 
mischief  may  be  the  occurrence  of  a  frank  hemoptysis.  Arrest  of  the 
disease  accompanied  by  fibrosis  of  the  lung  and  disappearance  of  the 
aspergillus  often  occurs. 

Physical  Signs. — In  the  early  stages  the  physical  signs  are  those  of 
bronchitis.  Later  there  is  evidence  of  localization,  usually  at  the  apex 
of  one  lung.  The  physical  signs  are  then  those  of  an  infiltration,  such 
as  occurs  in  tuberculosis. 

Diagnosis. — The  disease  is  to  be  distinguished  from  tuberculosis 
or  infections  of  a  similar  nature.  This  is  possible  only  by  examination 
of  the  sputum  for  organisms  other  than  the  tubercle  bacillus. 

1  "Etude  sur  l'aspergillose  chez  les  animaux  et  chez  l'homme,"  Paris,  1897. 

2  Trans.  Amer.  Climat.  and  Clin.  Assoc,  1915. 


390      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 


PULMONARY  SPOROTRICHOSIS 

Sporotrichosis  is  a  mycotic  affection  characterized  by  cutaneous  and 
internal  lesions.  It  is  caused  by  several  species  of  parasitic  fungi  belong- 
ing to  the  sporotrichosis  group.  The  first  case  was  described  by  Schenck 
in  America  in  1898.  Five  years  later  de  Beurmann  and  Ramond  re- 
ported the  first  case  in  France.  The  most  complete  study  of  the  affection 
is  to  be  found  in  the  monograph  by  de  Beurmann  and  Gougerot.1  From 
this  source  most  of  the  following  facts  have  been  obtained.  Infection  of 
the  lungs  with  one  of  the  Sporotrichosis  group  is  exceedingly  rare.  Ac- 
cording to  de  Beurmann  and  Gougerot  only  two  cases  with  bacteriological 
proof  have  been  reported,  namely,  those  by  Seguin  and  Chantemesse 
and  Rodriguez. 

Etiology. — The  most  common  site  of  the  infection  is  the  skin,  espe- 
cially that  of  the  hands  and  forearms.  More  rarely  it  occurs  on  a  mucous 
membrane.  Although  healthy  persons  may  be  attacked  it  occurs  most 
frequently  in  individuals  whose  resistance  has  been  lowered  by  some 
chronic  disease.  In  a  number  of  cases  an  abrasion  in  the  skin  has  been 
present  which  probably  serves  as  the  point  of  entrance.  As  the  sporo- 
trichum  is  found  on  various  vegetables,  infection  is  most  apt  to  occur  in 
those  handling  these  food  stuffs.  One  of  the  pulmonary  cases  ascribed 
her  trouble  to  the  inhalation  of  quantities  of  dust  in  the  coffee  mill  in 
which  she  was  employed. 

In  1912  Hamburger2  reported  58  cases;  two  years  later  Sutton3  added 
10  more  from  the  literature  and  5  personal  observations.  Of  the  73 
cases,  none  of  which  involved  the  lungs,  which  have  been  observed  in  this 
country,  68  came  from  the  region  comprising  the  Mississippi  River  basin. 
Whether  this  restriction  of  the  disease  to  a  certain  area  is  due  to  local 
conditions  or  a  failure  to  recognize  it  in  other  localities,  is  not  clear. 
The  same  thing  has  been  noted  in  regard  to  coccidoidal  granuloma  and 
blastomycosis. 

Morbid  Anatomy. — Little  is  known  as  to  the  pulmonary  changes. 
As  the  disease  is  chronic  and  may  last  for  a  year  or  more  it  is  probable 
that  fibroid  changes  in  the  lung  are  a  marked  feature.  Experimentally  de 
Beurmann  and  Gougerot  were  able  to  produce  a  variety  of  pulmonary 
lesions  in  animals.  These  consisted  of  broncho-pneumonic  areas,  small 
nodules,  fibroid  changes,  abscess  formation  and  in  some  instances  cavity 
formation  similar  to  that  seen  in  tuberculosis. 

Dissemination  from  the  skin  lesion  to  the  internal  organ  occasionally 
occurs.  The  skin  lesion,  as  described  by  de  Beurmann  and  Gougerot, 
may  be  one  of  three  types:  (1)  It  may  appear  in  the  form  of  multiple 
gummata  in  the  subcutaneous  tissues  in  various  parts  of  the  body. 
The  gummata  may  be  localized  in  one  region  of  the  body,  especially  the 
limbs,  or  be  widely  disseminated.  The  gumma  begins  as  a  small,  hard, 
movable  nodule  which  softens,  gradually  breaks  down,  and  discharges 
a  viscid  pus.  (2)  The  lesion  may  be  ulcerative  and  bear  a  strong  re- 
semblance to  cutaneous  tuberculosis.  There  may  be  a  small  localized 
group  of  ulcers.  The  usual  location  is  on  the  hands  and  arms.  (3) 
There  may  be  a  hard  chancroid-like  body,  eroded  on  the  surface. 

1  "Les  Sporotrichoses,"  1912. 

2  Jour.  Am.  Med.  Assoc,  Nov.  2,  1912. 

3  Ibid.,  Oct.  3,  1914. 


DISEASES    OF    THE    LUNGS  391 

Dissemination  occurs  through  the  lymphatics. 

Symptoms. — The  symptoms  of  the  proven  and  suspected  pulmonary 
cases  are  those  of  a  chronic  pulmonary  infection.  In  the  case  reported 
by  Chantemesse  and  Rodriguez,  a  woman,  aged  forty,  had  been  suffering 
from  pulmonary  symptoms  for  several  months.  She  had  a  painful  cough, 
mucilage-like  sputum,  which  later  became  yellowish  in  color  and  con- 
tained small  white  granules.  She  also  suffered  from  progressive  short- 
ness of  breath  and  pain  in  the  right  chest.  Physical  examination  showed 
impairment  of  the  percussion  note,  rough  breath  sounds  and  rales  at  the 
right  apex.  The  sputum  was  persistently  negative  for  tubercle  bacilli. 
Cultural  studies  of  the  sputum  showed  a  sporotrichum  closely  resembling 
that  described  by  de  Beurmann.  Agglutination  tests  confirmed  this 
finding.  The  woman  had  been  employed  in  a  coffee  mill.  She  asso- 
ciated her  trouble  with  the  inhalation  of  large  quantities  of  dust  in  her 
place  of  employment. 

Diagnosis. — This  is  possible  only  through  bacteriological  studies.  In 
regions  in  which  the  infection  is  known  to  exist  it  should  be  borne  in  mind 
■as  a  possible  cause  of  an  obscure  pulmonary  lesion. 


ACUTE  LOBAR  PNEUMONIA 
(Croupous  Pneumonia,  Fibrinous  Pneumonia,  Pleuro-pneumonia,  Lung  Fever) 

The  term  lobar  is  used  when  the  process  involves  an  entire  lobe  or 
part  of  a  lobe  without  healthy  tissue  intervening,  in  contradistinction  to 
lobular  pneumonia  which  occurs  in  isolated  or  confluent  patches.  The 
terms  fibrinous  or  croupous,  which  are  often  employed,  indicate  the  nature 
of  the  inflammatory  exudate.  The  name  pleuro-pneumonia  is  sometimes 
used  to  indicate  that  the  pneumonic  process  is  accompanied  by  a  pleurisy. 
By  the  laity  the  disease  is  often  referred  to  as  lung  fever  or  inflammation 
of  the  lungs. 

Etiology. — Considered  from  both  the  morbidity  and  the  mortality 
rates  croupous  pneumonia  is  decidedly  one  of  the  most  important  of  the 
acute  infectious  diseases.  As  a  cause  of  death  it  ranks  with  tubercu- 
losis of  the  lungs,  cardio-vascular  disease  and  nephritis. 

Age. — The  disease  may  occur  at  any  age  period.  Of  32,681  cases 
collected  from  the  literature  by  Norris  40.2  per  cent,  occurred  between 
the  tenth  and  thirtieth  years.  Up  to  the  sixth  year  the  morbidity 
rate  is  quite  high  while  the  mortality  rate  is  relatively  low.  Among 
those  of  advanced  years  the  incidence  is  very  high  and  the  death  rate 
equally  so. 

Sex. — In  adult  life  males  are  more  subject  to  pneumonia  than  females. 
Of  12,098  cases  collected  by  Musser  and  Norris,  73  per  cent,  were  males 
and  26  per  cent,  females.  Among  young  children  the  two  sexes  are  about 
equally  effected.  The  greater  incidence  among  adult  males  is  probably 
due  to  the  nature  of  their  occupations  which  in  many  instances,  offers 
greater  chances  for  exposure. 

Race.- — In  the  United  States  it  has  long  been  recognized  that  pneu- 
monia is  far  more  fatal  among  the  negroes  than  the  whites.  This  has 
been  noted  also  among  the  negroes  employed  in  the  construction  of  the 
Panama  Canal  and  among  the  negroes  working  in  the  mines  of  the  Rand, 
South  Africa.     In  both  these  places  it  has  been  noted  that  the  mortality 


392      DISEASES   OF   THE  BRONCHI,   LUNGS,    PLEURA,    AND   DIAPHRAGM 

from  pneumonia  is  highest  among  the  recent  arrivals  and  that  death 
rate  rapidly  diminishes  after  a  short  residence  in  the  community. 

Seasonal  Incidence. — For  years  the  relationship  between  cold  and 
pneumonia  has  been  regarded  as  a  close  one.  It  is  well  known  that  the 
disease  very  frequently  follows,  sometimes  within  a  few  hours,  a  wetting 
or  a  chilling  as  the  result  of  some  unusual  exposure.  The  pneumococcus 
is  a  frequent  inhabitant  of  the  upper  respiratory  tract  in  a  very  large 
proportion  of  healthy  people,  different  observers  obtaining  from  80  to 
90  per  cent,  positive  results.  Ordinarily  no  trouble  occurs  but  if  the 
individual  who  harbors  the  organism  happens  to  become  chilled  the 
resistance  of  the  bronchial  and  pulmonary  tissues  may  be  sufficiently 
lowered  to  permit  the  pneumococcus  to  gain  a  foothold.  In  other  words, 
cold  is  a  factor  and  not  the  actual  cause  of  the  disease.  Climate  does 
not  seem  to  exert  any  great  influence,  the  disease  occurring  with  equal 
frequency  in  both  hot  and  cold  countries.  Statistics,  however,  show  that 
the  incidence  of  the  disease  in  the  temperate  zone  is  unquestionably 
higher  during  the  winter  and  early  spring  months.  This  is  to  be  ascribed 
to  the  cold  in  the  winter  months  and  to  the  wide  variations  in  tempera- 
ture which  often  occur  in  the  early  spring.  In  Philadelphia  and  New 
York  and  the  Atlantic  Coast  generally,  the  highest  percentage  of  cases 
occurs  in  February  and  March. 

Influence  of  Insanitary  Conditions. — The  disease  is  more  common  in 
cities  than  in  the  country.  There  are  several  apparent  reasons  for  this. 
City  dwellers  are  confined  to  the  house  more  closely  than  those  in  the 
rural  districts  and  during  the  winter  months  the  urban  house  is  habitually 
overheated  thus  favoring  the  occurrence  of  catarrhal  processes  in  the 
air  passages. 

Bad  ventilation,  dark  rooms  and  overcrowding  which  characterize 
the  housing  conditions  of  a  large  portion  of  our  city  slums  are  undoubtedly 
factors  in  causing  pneumonia.  The  influence  of  overcrowding  is  well 
shown  by  Gorgas1  from  his  experience  at  Panama  in  1906  and  1907  and 
also  a  few  years  later  among  the  miners  of  the  Rand,  South  Africa.  Prior 
to  1907  the  negroes  working  on  the  Isthmian  Canal  were  housed  in 
barracks.  In  1907  the  negroes  were  removed  from  the  barracks  and 
allowed  to  scatter  along  the  line  of  the  Canal,  each  man  building  his  own 
hut  for  himself  and  family.  Coincidently  with  the  change  in  the  method 
of  housing  the  negroes,  there  was  an  immediate  drop  in  the  death  rate 
from  pneumonia.  In  1906  the  mortality  from  pneumonia  was  18.74 
per  thousand,  in  1907  it  was  10.65  per  thousand  and  in  the  years  succeed- 
ing up  to  and  including  1912  the  rate  did  not  exceed  2.60  per  thousand. 
This  Gorgas  attributes  to  the  change  in  housing  conditions.  His  investi- 
gation of  the  Rand  miners  also  seemed  to  indicate  that  the  crowded 
living  conditions  under  which  these  men  lived  had  an  undoubted  influence 
on  the  high  morbidity  and  mortality  rate  of  pneumonia.  Anders,  in 
his  study  of  the  distribution  of  pneumonia  in  Philadelphia,  found  that 
the  highest  mortality  from  the  disease  occurred  in  the  most  densely 
populated  wards. 

Epidemics. — There  is  now  sufficient  evidence  at  hand  to  indicate  that 

pneumonia  may,  in  some  instances,  be  transferred  from  person  to  person 

if  the  contact  is  a  close  one.     This  probably  accounts  for  the  epidemics 

which  have  been  noted  from  time  to  time  in  overcrowded  barracks,  jails 

1  Am.  Jour.  Med.  Sc,  1914,  lxii. 


DISEASES    OF    THE    LUNGS  393 

and  almshouses.  In  the  vast  majority  of  instances  pneumonia  is  to  be 
regarded  as  an  endemic  rather  than  an  epidemic  disease  and  for  the  most 
part  cases  occur  sporadically.  Occasionally,  however,  the  disease  at- 
tacks, within  a  short  time,  a  number  of  people  in  a  neighborhood  or 
institution  and  has  every  appearance  of  being  epidemic  in  character. 
Small  localized  epidemics  have  been  noted  also  in  institutions  and  for 
this  reason  many  hospitals  isolate  their  pneumonia  patients. 

The  belief  that  pneumonia  is  contagious  is  strengthened  by  the  obser- 
vations of  Dochez  and  Avery.1  Although,  as  previously  stated,  pneumo- 
cocci  exist  in  the  mouth  of  many  healthy  people  such  organisms  can  be 
distinguished  from  the  more  virulent  ones  which  give  rise  to  severe  forms 
of  lobar  pneumonia.  Dochez  and  Avery  found  that  healthy  persons 
intimately  associated  with  cases  of  lobar  pneumonia  harbored  the  disease- 
producing  types  of  pneumococci  and  that  in  every  instance  the  organism 
isolated  corresponded  in  type  with  that  of  the  infected  individual. 
Convalescents  may  carry  virulent  pneumococci  for  some  time. 

Personal  Conditions.- — While  robust  healthy  men  are  frequently 
attacked  by  pneumonia,  individuals  who  have  become  debilitated  through 
disease  or  dissipation  are  far  more  susceptible  to  the  disease.  Among 
those  suffering  from  the  various  chronic  diseases  such  as  arterio-sclerosis, 
nephritis,  heart  disease,  malignant  disease,  etc.,  an  attack  of  croupous 
pneumonia  is  the  terminal  event  in  a  very  large  number  of  cases.  The 
extreme  susceptibility  of  the  alcoholic  to  a  fatal  attack  of  pneumonia  has 
long  been  recognized. 

Trauma. — Pneumonia  has  been  noted  in  a  small  percentage  of  cases 
to  follow  some  injury  of  the  chest  wall  without  there  being  any  injury 
of  the  lung  itself. 

Previous  Attacks. — Lobar  pneumonia  is  common  with  diphtheria  and 
erysipelas,  differs  from  the  other  infectious  diseases  in  that  one  attack 
does  not  afford  protection  against  a  recurrence  of  the  trouble.  No  other 
disease  is  so  prone  to  recur  in  the  same  individual.  Two  and  three 
attacks  have  been  noted  frequently  and  not  a  few  instances  are  on 
record  of  individuals  who  have  had  -ten  or  more  attacks.  In  the  oft- 
quoted  case  of  Benjamin  Rush  no  less  than  28  attacks  occurred. 

Post-operative  Pneumonia. — It  is  not  altogether  clear  whether  the 
combined  effect  of  an  anesthetic,  particularly  ether,  and  operative  inter- 
ference are  factors  in  the  production  of  lobar  pneumonia.  In  a  small 
percentage  of  cases  pneumonia  undoubtedly  does  follow  the  operation. 
Laparotomies  seem  to  be  followed  by  pneumonia  more  frequently  than 
is  the  case  when  other  portions  of  the  body  are  operated  upon.  It  is 
to  be  borne  in  mind,  however,  that  a  latent  and  unrecognized  pneumonia 
may  have  been  present  at  the  time  of  the  operation. 

The  generally  accepted  theory  as  to  the  cause  of  post-operative  pneu- 
monia is  that  one  or  all  of  the  following  factors  may  be  at  fault:  (1) 
The  patient  may  become  chilled  on  the  operating  table;  (2)  that  excre- 
tions from  the  mouth  may  become  aspirated  into  the  lung;  and  (3)  that 
the  infection  may  arise  from  an  unsterilized  inhaler. 

Inhalation  and  Aspiration  Pneumonia. — Lobar  pneumonia  may  arise 
as  the  result  of  the  aspiration  of  fluids  or  solid  material  into  the  lung  or 
as  the  result  of  the  inhalation  of  irritant  dusts  or  chemicals.     But  as  a 

1  Jour.  Exp.  Med.,  xxii,  1915. 


394      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

rule  the  above-mentioned  accidents  are  followed  by  broncho-pneumonia 
rather  than  the  lobar  type  of  the  disease. 

Occupation. — This  is  often  given  as  a  predisposing  cause  of  pneu- 
monia. The  effect  of  any  particular  occupation  on  the  production  of 
pneumonia  is  problematical.  If  the  sanitary  conditions,  which  include 
proper  ventilation,  are  good  the  occurrence  of  pneumonia  among  the 
workers  will  be  less  than  if  the  reverse  be  true.  It  is  also  to  be  borne  in 
mind  that  the  sanitary  arrangements  of  the  working  place  may  be  perfect 
while  the  home  conditions  are  very  bad. 

Bacteriology. — The  exciting  cause  of  lobar  pneumonia,  in  a  large 
proportion  of  cases,  is  the  pneumococcus.  This  organism  is  also  known 
as  the  diplococcus  pneumoniae  and  micrococcus  lanceolatus.  In  a  few 
instances  the  pneumonia  is  caused  by  a  streptococcus  or  the  influenza 
bacillus ;  more  rarely  Friedlander's  bacillus  is  the  organism  found.  These 
organisms  may  occur  alone  or  in  association  with  the  pneumococci.  - 

For  many  years  it  has  been  a  matter  of  clinical  observation  that 
epidemics  of  pneumonia  showed  marked  differences  in  the  mortality  rate 
and  that  even  in  the  same  epidemic  the  virulence  of  the  infection  varied 
greatly.  To  this  variability  of  the  disease  may  be  ascribed  some  of  the 
favorable  reports  which  have  appeared  from  time  to  time  on  the  effect 
of  some  particular  method  of  treatment. 

As  the  result  of  work  by  Neufeld  and  by  Cole  and  his  co-workers, 
Dochez,  Avery,  and  Gillespie,  at  the  Rockefeller  Hospital,  it  has  been 
shown  that  there  are  several  varieties  of  pneumococci  and  that  these 
can  be  distinguished  one  from  the  other  by  immunological  reactions. 
Thus  by  testing  pneumococci  with  the  serum  of  animals  immunized 
against  them,  it  has  been  found  that  they  may  be  divided  into  at  least 
four  groups.  According  to  Cole1  all  the  organisms  of  group  I  are  alike 
so  far  as  their  immune  reactions  are  concerned.  The  same  is  true  of 
organisms  of  group  II.  In  group  III  (pneumococcus  mucosus)  the  organ- 
isms also  show  peculiar  immunity  reactions,  and  in  addition,  they  differ 
from  those  of  the  preceding  groups  in  that  they  have  larger  capsules  and 
form  a  sticky  exudate  in  animals.  In  group  IV  are  placed  the  remaining 
organisms  which  are  found  to  show  no  common  immunity  reactions  and 
are,  in  addition,  much  less  virulent. 

Although  the  clinical  features  show  no  marked  differences,  the  severity 
of  the  pneumonia  varies  greatly  with  the  type  of  organism.  The  fol- 
lowing figures  given  by  Cole2  show  the  relative  frequency  and  the  mor- 
tality of  pneumonia,  due  to  the  different  types  of  pneumococci,  observed 
in  the  Rockefeller  Hospital,  New  York. 


-■-.,•  i-i  %'        c  Percentage  inci-  ,rnFi„i;(„ 

Etiological  agent  I\o.  of  cases  dence  Mortality 


35 .0  25 . 0 

33 . 5  29 . 0 


9.0  45 . 0 


Pneumococcus  type  1 7S 

Pneumococcus  type  II 75 

Pneumococcus  type  III 22 

Pneumococcus  tvpe  IV 4S  21.5  12 . 5 

Total '. 

223 

1  Monthhj  Bulletin  N.  Y.  Dept.  of  Health,  February,  1916. 

2  Trans.  Assoc.  Am.  Phys.,  1915,  p.  234. 


DISEASES    OF    THE    LUNGS 


395 


In  a  study  of  195  cases  at  the  Pennsylvania  Hospital,  Philadelphia, 
Richardson1  obtained  the  folio  wins;  results: 


Etiological  agent 

XT        r                       Percentage  inci- 
No.  of  cases                      de  Jre 

Mortality 

Pneumococcus  tvpe  I 

Pneumococcus  type  II 

Pneumococcus  tvpe  III 

Pneumococcus  type  IV 

Total 

60 
39 
13 

83 

195 

31 

20 

6 

43 

30 
25 

50 
12 

It  will  be  seen  that  the  figures  in  the  two  series  are  very  similar  and 
that  the  majority  of  the  cases  are  due  to  types  I  and  II,  and  that  the 
mortality  ranges  from  25  to  30  per  cent.  Infection  with  type  III  is  the 
least  frequent,  a  fortunate  circumstance,  as  the  mortality  in  this  group 
is  very  high.  As  Cole  points  out  the  frequency  of  cases  due  to  type  IV 
probably  varies  in  different  places  and  at  different  times.  The  mortality 
in  group  IV  is  not  high;  in  some  series  it  has  been  as  low  as  6  per  cent. 

The  separation  of  pneumococci  into  distinct  groups  has  been  of  great 
practical  value. 

1.  A  knowledge  of  the  type  of  organism  has  made  it  possible  to  fore- 
tell the  probable  outcome  of  the  disease.  Thus  if  the  agglutination  test 
shows  the  presence  of  type  I  or  II  the  use  of  a  specific  serum  is  possible; 
if  type  III  is  present  the  outlook  is  bad;  if  the  organism  belongs  to  type 
IV  the  chances  are  greatly  in  favor  of  the  patient.  To  determine  the 
type  a  mouse  is  injected  with  some  of  the  sputum  and  6  hours  later 
some  of  the  peritoneal  fluid  is  removed  and  an  agglutination  test  is  done. 
This  may  determine  the  type  at  once.  If,  however,  no  reaction  occurs 
the  mouse  is  allowed  to  die,  this  taking  place  within  24  hours,  and  the 
agglutination  test  is  again  done.  Cultural  peculiarities  may  be  an  aid 
also.  It  is  needless  to  say  that  this  is  possible  only  in  a  hospital  with  a 
well-equipped  laboratory. 

2.  It  has  been  known  for  some  years  that  pneumococci  are  present 
in  the  mouths  of  healthy  individuals  in  a  very  high  percentage  of  cases; 
some  observers  have  found  as  high  as  80  or  90  per  cent,  of  normal  indi- 
viduals harboring  these  organisms  in  the  mouth.  This  has  made  it 
difficult  to  understand  how  these  bacteria  can  cause  pneumonia  unless 
there  is  some  other  primary  or  predisposing  factor.  Cole  offers  the 
following  explanation:  For  a  pulmonary  pneumococcus  infection  to 
occur,  at  least  two  factors  are  probably  responsible.  First,  the  condition 
in  the  host,  local,  general  or  both,  must  be  favorable  for  infection;  and 
second,  an  organism  of  suitable  virulence  must  be  present.  With  organ- 
isms of  the  type  ordinarily  found  in  the  mouth  (type  IV),  probably  the 
changes  in  the  patient  are  of  chief  importance.  With  pneumococci  of  the 
fixed  types  (I,  II,  and  III),  however,  the  presence  of  the  organism  is  of 
great  importance,  and  may  even  determine  the  onset  of  the  illness. 
Even  in  this  case,  however,  changes  in  the  resistance  of  the  patients  arc 
probably  of  some  importance,  as,  under  certain  circumstances,  healthy 
persons  may  carry  these  fixed  types  without  becoming  themselves  in- 
fected. This  last-mentioned  group  may  be  compared  to  the  so-called 
diphtheria  and  typhoid  carriers. 

1  Trans.  Assoc.  Am.  Phys.,  1915,  p.  234. 


396       DISEASES    OF   THE  BRONCHI,    LUNGS,    PLEURA,    AXD    DIAPHRAGM 

3.  The  most  important  outgrowth  of  this  work  is  that  which  relates 
to  treatment.  It  is  too  early  to  speak  with  certainty  but  the  results  so 
far  obtained  with  the  serum  produced  at  the  Rockefeller  Hospital  are 
extremely  encouraging.  Cole  states  that  the  most  successful  results 
have  been  obtained  in  cases  treated  with  serum  of  type  I.  Among  the 
cases  so  treated  the  mortality  was  only  8  per  cent.,  as  contrasted  with  25 
per  cent,  in  the  untreated  cases.  The  results  obtained  in  a  few  cases 
treated  with  serum  of  type  II  have  been  much  less  encouraging.  There 
is  no  specific  treatment  for  either  type  III  or  type  IV. 

Morbid  Anatomy. — As  the  result  of  careful  bacteriological  studies  it 
is  now  apparent  that  croupous  pneumonia  is  a  generalized  infection  with 
a  local  manifestation.  And  while  the  brunt  of  the  infection  is  borne  by 
the  lung  the  diplococcus  may  be  found  in  various  other  portions  of  the 
body  as  well  as  in  the  circulating  blood.  We  ha\Te  already  alluded  to  the 
fact  that  a  very  high  percentage  of  healthy  individuals  harbor  the 
diplococcus  in  the  upper  air  passages  and  that  under  ordinary  conditions 
the  germ  is  innocuous. 

If,  however,  the  individual  becomes  chilled  or  is  the  victim  of  some 
chronic  disease  the  natural  defenses  are  incapable  of  maintaining  the 
upper  hand.  The  result  is  that  the  diplococcus  is  unleashed,  as  it  were, 
and  permitted  to  grow  unrestrained. 

Since  the  time  of  Laennec  it  has  been  customary  to  describe  the 
changes  which  take  place  in  the  lungs  as:  (1)  the  stage  of  engorgement; 
(2)  the  stage  of  red  hepatization;  and  (3)  the  stage  of  gray  hepatization. 
In  accepting  this  classification,  however,  it  is  to  be  understood  that  the 
development  of  the  different  stages  of  the  morbid  process  is  not  always 
uniform.  And  while  for  the  most  part  the  lesion  may  be  predominantly 
that  of  engorgement  or  red  or  gray  hepatization,  two  or  all  three  of  these 
stages  may  be  present  in  the  same  lung. 

In  the  stage  of  engorgement  the  affected  portion  of  the  lung  is  deep 
red  in  color,  heavier  than  normal  and  often  slightly  edematous.  Although 
the  air  content  is  diminished  the  tissue  still  crepitates  and  excised  por- 
tions will  float  in  water.  On  section  there  is  an  abundant  hemorrhagic 
exudate.  The  capillaries  are  distended  and  the  alveolar  epithelium 
swollen  and  occasionally  desquamated. 

The  second  stage  or  that  of  red  hepatization  is  characterized  by  coagu- 
lation of  the  fibrinous  exudate  and  the  affected  area  has  become  of  the 
consistence  and  appearance  of  liver,  hence  the  name  hepatization.  In 
this  stage  the  lung  is  swollen  and  heavy;  pits  on  pressure;  is  very  friable 
and  readily  broken.  It  is  completely  airless  and  excised  portions  sink 
in  water.  On  section  the  cut  surface  is  dry  and  presents  a  granular  ap- 
pearance due  to  the  projection  of  small  fibrinous  plugs  in  the  air  cells. 
A  tenacious,  creamy,  grayish-red  fluid  containing  granular  masses  can 
be  scraped  off  the  cut  surface.  Fibrinous  casts  are  often  found  in  the 
smaller  bronchi.  Microscopically  the  air  cells  are  seen  to  be  filled  with 
a  coagulated  exudate  in  which  there  are  swollen  and  desquamated  epi- 
thelium, red  blood  cells  and  a  few  leukocytes.  A  round-celled  infiltra- 
tion is  also  seen  about  the  vessels  in  the  interlobular  septa. 

The  transition  from  the  stage  of  red  to  gray  hepatization  is  gradual. 
The  red  color  is  replaced  by  a  yellowish  or  ashen  gray  color.  Here  and 
there  are  often  to  be  noted  dark  red  or  reddish  gray  areas  and  if  in  addition 
anthracosis  is  at  all  marked  the  cut  surface  presents  a  mottled  appearance 


DISEASES    OF    THE    LUNGS 


397 


(Fig.  272) .  The  lung  is  swollen  and  firm  to  the  touch  and  is  often  indented 
with  the  impressions  of  the  ribs.  The  tissue  is  more  friable  and  more 
easily  torn  than  in  the  second  stage. 

The  overlying  pleura  is  dull  and  granular  in  appearance  and  covered 
with  a  fibrinous  exudate.  A  small  effusion  may  be  present  (see  Fig. 
315).  Inflammatory  changes  in  the  pleura  are  constantly  present  in 
lobar  pneumonia  except  in  those  cases 
in  which  the  lesion  is  centrally  located 
and  does  not  approach  the  periphery 
of  the  lung. 

On  section  the  cut  surface  of  the 
lung  has  become  moister  and  the 
granular  appearance  less  marked. 
The  fluid  scraped  from  the  surface 
of  the  section  is  more  abundant,  milky 
and  puriform.  Microscopically  the 
air  cells  are  seen  to  be  packed  with 
leukocytes  while  the  fibrin  and  the  red 
blood  cells  have  largely  disappeared. 
In  some  instances  the  tissue  is  very  ' 
soft  and  freely  exudes  a  purulent 
exudate  (purulent  infiltration)  and 
small  abscesses  may  develop. 

The  anemic  appearance  of  the 
affected  area  during  the  stage  of  gray 
hepatization  is  due  in  part  to  the  large 
number  of  leukocytes  and  in  part  to 
the  pressure  on  the  capillary  vessels. 

While  the  majority  of  cases  follow 
the  sequence  of  events  described 
above,  each  stage  lasting  from  two 
to  three  days,  the  process  may 
terminate  in  two  or  three  days  instead . 
of  being  prolonged  for  a  week  or 
more.  In  children,  the  aged,  and  the 
asthenic,  the  amount  of  fibrin  pro- 
duced may  be  small  and  the  alveoli 
but  slightly  distended,  so  that  the 
usual  dry,  granular  appearance  of  the 
lung  is  not  observed  (Adami). 

Resolution. — The  first  evidence 
pointing  to  the  stage  of  resolution 
is  a  breaking  up  of  the  fibrin  and 
fatty  degeneration  of  the  leukocytes. 
The  lung  becomes  smaller,  has  a  boggy  feel  and  the  pleura  becomes  re- 
laxed and  thrown  into  folds.  On  section  the  surface  is  yellowish  in 
color,  very  moist  and  a  creamy,  almost  purulent  fluid  can  be  squeezed 
out.  The  softened  exudate  is  removed  partly  by  being  expectorated  and 
partly  by  absorption;  the  latter  is  probably  the  more  important  as  the 
exudate  disappears  in  cases  in  which  both  cough  and  expectoration  are 
entirely  absent.     The  dissolving  of  the  exudate  is  due  to  autolysis. 

The  coagulated  albumen  is  broken  up  into  soluble  albuminoids  and 


Fig. 


!72. — Gray  hepatization  with 
anthracosis. 


398      DISEASES   OF   THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

further  decomposition  products  through  the  action  of  a  ferment  that  is 
probably  given  off  by  the  leukocytes  (Strumpell).  Cook,  in  Osier's 
Clinic,  has  shown  that  the  excretion  of  the  dissolved  exudate  takes  place 
through  the  kidneys  as  shown  by  the  excessive  nitrogen  excretion  in  the 
urine. 

With  the  removal  of  the  exudate  the  desquamated  epithelium  in  the 
alveoli  are  replaced  by  regeneration  from  those  remaining  intact;  gradu- 
ally there  is  a  complete  restoration  to  the  normal.  In  the  vast  majority 
of  cases,  especially  in  young,  healthy  individuals,  complete  resolution 
takes  place  uninterruptedly.  In  a  small  proportion  of  cases  the  dis- 
eased area  instead  of  undergoing  a  normal  involution  becomes  the  site 
of  an  abscess,  a  gangrenous  process,  or  fibroid  induration. 

Site  of  the  Disease. — It  has  been  shown  in  every  series  of  cases  of 
lobar  pneumonia  that  the  lower  lobes  of  the  lungs  are  the  parts  most 
frequently  affected  and  that  the  right  lower  lobe  is  slightly  more  vulner- 
able than  the  left.  The  excess  of  frequency  of  the  affection  of  the  right 
over  the  left  lung  as  a  unilateral  affection,  and  independently  of  the  loca- 
tion of  the  lesion,  may  be  regarded  as  occurring  in  the  proportion  of  about 
3  to  2.  The  distribution  of  the  lesions  is  well  illustrated  in  Jiisgensen's1 
large  series  of  6666  cases:  right  lung,  3580  cases:  left  lung,  2548  cases; 
both  lungs,  538  cases.  Involvement  of  the  upper  lobes  occurs  more  fre- 
quently in  children  and  in  those  of  advanced  years  than  in  the  middle 
periods  of  life.  When  the  disease  attacks  both  lungs  it  is  the  two  lower 
lobes  that  are  usually  affected  but  bilateral  lesions  may  occur  in  both 
apices  or  in  one  apex  and  one  lower  lobe.  Rarely  both  lungs  may  be 
extensively  involved.  In  a  case  seen  at  the  Philadelphia  General  Hospital 
death  occurred  on  the  third  day  and  at  the  autopsy  both  lungs,  from  apex 
to  base,  were  found  to  be  in  the  stage  of  red  hepatization. 

The  unaffected  portion  of  the  lobe  may  show  no  change  but  is  very 
commonly  congested  and  edematous.  The  uninvolved  lobes  both  on 
the  affected  and  the  unaffected  side  may  be  dry  and  bloodless  or  may 
show  evidences  of  congestion. 

Associated  Lesions. — The  mucous  membrane  of  the  bronchi  is  more 
or  less  congested  and  the  smaller  tubes  are  usually  blocked  with  a  fibrin- 
ous exudate.  In  some  instances  even  the  large  bronchi  are  filled  with  the 
exudate  constituting  what  is  known  as  massive  pneumonia.  The  bron- 
chial lymph  nodes  are  constantly  swollen. 

Except  in  cases  of  central  pneumonia  the  pleura  is  always  involved. 
The  portion  overlying  the  pulmonary  lesion  is  dull,  and  granular  in 
appearance  and  covered  with  lymph.  A  slight  excess  of  serofibrinous 
or  fibrinopurulent  exudate  is  often  present  and  occasionally  becomes 
sufficiently  large  to  constitute  a  true  empyema.  The  occurrence  of  the 
latter  is  relatively  common  in  children. 

Pericarditis. — Based  on  autopsy  findings  pericarditis  is  far  more 
common  than  clinical  data  would  indicate.  During  life  pericarditis  is 
almost  constantly  overlooked.  This  is  well  illustrated  by  figures  given 
by  Cowan  who  reports  a  post-mortem  incidence  of  12.6  per  cent,  as  con- 
trasted with  1.2  per  cent,  from  the  wards.  The  pericardium  may  be 
involved  as  a  part  of  the  general  infection  but  in  most  instances  the 
pericardial  infection  arises  apparently  as  the  result  of  direct  extension 

1  Ziemssen's  "Handbuch  d.  Spec.  Path.  u.  Xer.,*'  1874. 


DISEASES    OF   THE    LUNGS  399 

from  the  lung.  Rarely  a  pericardial  effusion,  serofibrinous  or  purulent 
in  character,  may  occur. 

Endocarditis  is  not  often  noted  during  life  but  at  the  autopsy  table 
it  is  not  an  infrequent  finding.  In  a  series  of  100  post-mortem  cases  Osier 
noted  the  presence  of  endocarditis  in  16  instances.  The  lesion  is  more 
commonly  of  the  ulcerative  type. 

Meningitis. — Occasionally  meningitis  occurs  during  the  course  of 
lobar  pneumonia.  The  frequency  with  which  it  is  encountered  varies 
widely.  Osier  noted  the  presence  of  meningitis  in  8  of  100  autopsied 
cases  while  Pearce  observed  but  2  out  of  121  cases. 

Of  the  more  unusual  complications  mention  should  be  made  of  peri- 
tonitis, otitis  media,  arthritis,  parotitis  and  abscess  formation  in  various 
portions  of  the  body.  In  addition  there  may  be  associated  with  the 
disease  diphtheritic  inflammation  of  the  mucous  membrane  of  the 
stomach,  intestines  or  mouth. 

In  common  with  the  other  infectious  diseases  degenerative  changes 
are  usually  evident  in  the  heart,  liver  and  kidneys  and  the  spleen  is  often 
enlarged  and  softened. 

Symptoms. — The  incubation  period  of  pneumonia  is  not  absolutely 
known.  The  disease  has  been  observed  to  develop  within  a  day  or  two 
after  a  traumatic  injury  to  the  chest.  In  those  instances  in  which  the 
disease  assumes  the  proportions  of  an  epidemic  seven  or  eight  days  may 
elapse  between  the  time  of  exposure  and  the  development  of  the 
trouble. 

In  the  great  majority  of  cases  pneumonia  both  in  its  mode  of  onset 
and  in  the  symptoms  which  characterize  its  course,  presents  a  typical 
picture.  It  is  estimated  that  in  80  per  cent,  of  cases  the  onset  occurs 
suddenly.  In  20  per  cent,  it  is  indefinite  and  the  actual  occurrence  of  the 
disease  is  preceded  by  prodromes.  In  many  of  these  cases  there  is  a 
history  of  a  slight  respiratory  infection  which  differs  in  no  way  from  an 
ordinary  "cold."  This  may  have  been  present  for  several  days  or  even 
a  week  or  longer  when  the  pneumonic  process  suddenly  manifests  itself. 
In  other  instances  the  patient  may  complain  for  several  days  of  a  feeling 
of  lassitude,  headache,  pain  in  the  limbs,  chilliness  or  slight  fever.  An 
insidious  onset  is  frequently  seen  in  pneumonia  as  it  occurs  in  the  aged, 
in  alcoholics  and  as  a  terminal  infection  in  chronic  diseases. 

In  frank,  typical,  lobar  pneumonia  the  onset  is  sudden  and  character- 
ized by  a  severe  chill  which  may  last  for  as  long  as  a  half  an  hour;  or  in- 
stead of  the  initial  rigor  the  patient  may  complain  of  chilliness  and  pain 
in  the  side.  Coincidently  with  the  chill,  fever  appears.  By  the  end  of 
the  first  day  or  the  beginning  of  the  second  the  clinical  picture  in  a  typical 
case  is  characteristic.  The  patient  is  breathing  more  rapidly  than  usual; 
complains  of  pain  in  the  side,  the  pain  in  some  instances  being  almost  un- 
bearable; and  there  is  a  frequent,  partially  suppressed  cough  which  for  a 
day  or  so  is  unproductive.  By  the  second  or  third  clay  the  patient  expec- 
torates the  characteristic  sputum.  This  may  be  bright  red  but  more 
commonly  is  brownish-red  or  rusty  in  appearance  and  extremely  tena- 
cious. The  gummy,  viscid  character  of  the  sputum,  which  renders  its 
expulsion  difficult  and  causes  it  to  adhere  to  the  side  of  the  sputum  cup, 
is  pathognomic  of  croupous  pneumonia. 

The  disease  has  an  average  duration  of  from  five  to  ten  days  when, 
in  a  little  over  half  of  cases,  it  abruptly  terminates  by  crisis. 


400      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

Special  Symptoms. — Fever. — A  rise  in  the  temperature  occurs  at 
the  time  of  the  chill  and  may  reach  the  fastigium  within  12  to  24  hours. 
In  some  instances  the  fever  may  increase  gradually  for  a  couple  of  days. 
The  temperature  of  pneumonia  is  continuous  in  type  with  slight  evening 
remissions  which  may  not  amount  to  more  than  one  degree.  In  the 
average  case  the  temperature  ranges  between  103°  and  105°F.  during  the 
course  of  the  disease  when  it  abruptly  falls  by  crisis  (Fig.  273).  About 
70  per  cent,  of  cases  may  be  expected  to  terminate  in  from  five  to  ten 


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Fig.  273. — Crisis  in  lobar  pneumonia.     Note  the  drop  in  the  pulse  and  respiratory  rates 
following  the  fall  in  the  temperature. 


days.  Occasionally  cases  are  encountered  in  which  the  disease  termi- 
nates as  early  as  the  third  day  and  more  often  it  may  be  prolonged  for 
two  weeks  or  more.  In  cases  of  long  duration  the  temperature  usually 
subsides  by  lysis  (Fig.  274).  In  not  a  few  cases  there  is  apt  to  occur  in 
the  middle  of  the  course  of  the  disease  a  slight  drop  in  the  temperature 
after  which  it  again  arises.  This  is  known  as  a  pseudo-crisis  (Fig.  275) . 
Among  1854  collected  cases  a  pseudo-crisis  was  noted  in  172  or  9.8  per 
cent.  (Norris).  Occasionally  just  prior  to  the  crisis  the  fever  may  increase 
slightly. 


DISEASES    OF    THE    LUNGS 


401 


While  as  a  rule  hyperpyrexia  is  associated  with  fatal  cases  recovery 
has  followed  very  high  temperatures — 107°  to  109°F.  A  fairly  high 
degree  of  fever,  from  103°  to  105°F.,  is  not  a  bad  sign  but  relatively  low 
temperatures  are  very  commonly  associated  with  fatal  cases.  A  tem- 
perature of  100°F.  or  less  is  very  frequently  seen  in  pneumonia  as  it 


Fig.  274. — Fall  of  temperature  by  lysis. 

occurs  in  the  aged,  in  the  debilitated  and  in  those  with  an  overwhelming 
infection. 

Pain  in  the  chest  is  one  of  the  most  constant  symptoms  of  pneu- 
monia, some  observers  having  noted  its  presence  in  as  high  as  90  per  cent. 
of  cases.  It  may  be  the  first  symptom  noticed,  in  some  cases  preceding 
the  chill;  on  the  other  hand,  it  may  not  make  itself  manifest  until  the 


Fig.  275. — Pseudo-crisis  in  pneumonia. 

third  or  fourth  day  of  the  disease.  The  pain  may  disappear  in  a  day 
or  so  but  as  a  rule  continues  throughout  the  attack.  In  the  frank  pneu- 
monia of  adults  the  pain  is  usually  sharp  and  lancinating  in  character 
and  in  some  instances  is  so  severe  as  to  be  almost  unbearable.  In  central 
and  apical  pneumonias  and  in  children  pain  may  be  very  slight  or  entirely 

26 


402      DISEASES   OF   THE  BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

absent.  Xor  is  it  much  in  evidence  in  senile  or  asthenic  pneumonias. 
In  delirious  patients  pain  is  not  complained  of  at  all.  As  a  rule  the  pain 
corresponds  to  the  site  of  the  consolidation  but  not  infrequently  it  is 
referred  to  the  region  of  the  nipple  on  the  affected  side.  Rarely  pain 
may  be  complained  of  on  the  unaffected  side.  Most  important  to  bear 
in  mind  is  the  fact  that  the  pain  produced  by  pneumonia  may  be  re- 
ferred to  the  abdomen  and  thus  simulate  appendicitis  or  some  other 
abdominal  lesion.  Failure  to  recognize  the  true  source  of  the  pain  has, 
in  not  a  few  instances,  led  to  the  performance  of  a  laparotonry.  Chatard 
noted  abdominal  pain  51  times  in  658  pneumonia  patients  (7.7  per  cent.) 
and  Griffith  has  recorded  a  number  of  instances  in  which  it  has  occurred 
in  children. 

While  severe  pain  in  the  chest  is  not  pathognomonic  of  pneumonia 
its  occurrence  is  significant  if  the  pain  is  greatly  increased  by  breathing, 
coughing  and  talking,  or  if  aggravated  by  moving  about.  In  some  in- 
stances the  chest  wall  over  the  site  of  the  consolidation  is  hyperesthetic, 
the  patient  often  complaining  bitterly  when  the  region  is  percussed.  Im- 
mobilization of  the  affected  side  often  relieves  the  pain  by  limiting  the 
respiratory  excursion  and  thus  preventing  the  inflamed  surfaces  of  the 
pleura  from  rubbing  together. 

Headache  is  usually  experienced  at  the  onset  of  the  disease.  In  some 
instances  it  is  very  severe.     Earache  may  also  be  complained  of. 

Respiratory  Symptoms. — Acceleration  of  the  respiratory  rate  may  be 
one  of  the  earliest  symptoms  of  pneumonia  especially  when  the  disease 
occurs  as  a  terminal  infection  in  the  aged  or  in  those  suffering  from  some 
chronic  affection.  The  type  of  the  breathing  is  of  the  greatest  diag- 
nostic importance.  The  respirations  are  short  and  shallow  and  often 
accompanied  by  an  "  expiratory  grunt "  and  inspiratory  dilatation  of  the 
alse  nasi.  The  respiratory  rate  is  almost  invariably  quickened.  It  is 
rarely  under  30  and  in  adults  the  rate  may  be  as  high  as  60  or  70  per 
minute.  In  children  the  respiratory  rate  may  be  100  or  more.  Quicken- 
ing of  the  respiratory  rate  is  due  to  several  causes,  namely:  to  a  limita- 
tion of  the  respiratory  excursion  due  to  pain,  which  is  especially  noticeable 
when  one  of  the  lower  lobes  is  involved;  to  the  amount  of  pulmonary 
tissue  consolidated;  and  to  fever,  toxemia  or  cyanosis.  In  those  cases 
in  which  pain  is  the  chief  factor  the  respirations  tend  to  become  deeper 
and  slower  with  the  subsidence  of  the  pain;  on  the  other  hand,  if  the 
involvement  extends  or  if  the  toxemia  increases  in  severity  the  respiratoiy 
rate  will  increase  in  rapidity.  While  extreme  rapidity  of  the  respiratoiy 
rate  cannot  be  regarded  in  all  cases  as  of  serious  significance  it  is  to  be 
noted  that  a  fatal  issue  occurs  more  frequently  in  patients  in  whom  the 
rate  is  above  50.  The  exceptions  to  this  general  rule  are  cases  in  which 
the  rapid  and  shallow  breathing  is  caused  by  severe  pain.  Dyspnea  may 
be  present  in  conjunction  with  the  increased  respiratory  rate.  It  is  usually 
indicative  of  a  profuse  bronchial  catarrh,  edema  of  the  lungs  or  some  com- 
plication which  restricts  the  expansion  of  the  lung,  such  as  an  effusion. 

Cough. — In  the  atypical  forms  of  pneumonia,  such  as  sometimes  occur 
in  the  aged,  in  alcoholics  and  in  those  with  apical  lesions,  cough  is  some- 
times absent,  but  in  practically  all  cases  of  frank  pneumonia  in  adults 
cough  is  a  prominent  symptom.  In  those  cases  in  which  the  pneumonia 
is  preceded  by  a  "cold"  the  cough  is  already  present  at  the  time  of  the 
chill.     When  the  disease  is  ushered  in  with  a  sudden  onset  the  cough 


DISEASES    OF    THE    LUNGS  403 

occurs  with  or  very  shortly  after  the  chill  and  in  the  beginning  is  unpro- 
ductive and  often  paroxysmal.  Owing  to  the  associated  pleurisy  the 
act  of  coughing  greatly  intensifies  the  pain  and  for  this  reason  the  patient 
attempts  to  suppress  or  smother  the  cough.  In  the  course  of  one  to 
three  days  expectoration  appears  and  the  cough  may  lessen  in  severity. 
On  the  other  hand,  the  cough  may  increase  in  severity  and  greatly  tax 
the  patient's  strength.  The  sudden  disappearance  of  the  cough  is  to 
be  looked  on  as  of  grave  import  as  it  not  infrequently  indicates  the 
onset  of  exhaustion  or  coma. 

Sputum. — The  character  of  the  sputum  constitutes  the  one  feature 
of  pneumonia  that  may  be  regarded  as  pathognomonic.  Often  absent 
for  the  first  day  or  so,  it  appears  first  as  a  frothy,  white  substance,  which 
may  be  streaked  with  blood.  In  the  course  of  a  few  hours,  however,  it 
assumes  its  characteristic  appearance.  In  color  it  is  rustj^  or  brick-dust 
in  appearance,  due  to  the  admixture  of  blood  and  the  fibrinous  exudate. 
Of  more  importance  is  the  consistency.  Typical  pneumonic  sputum 
is  semitransparent,  viscid  and  extremely  tenacious,  being  expelled  with 
difficulty  and  adhering  to  the  side  of  the  sputum  cup.  As  the  disease 
progresses  and  the  stage  of  gray  hepatization  is  reached,  the  sputum  loses 
its  sanguinolent  appearance  and  becomes  yellowish  and  finally  white. 
At  times  it  has  a  greenish  tinge.  Instead  of  being  thick  and  tenacious, 
the  sputum  may  be  watery  and  of  a  brownish  color,  resembling  prune 
juice.  Sputum  of  this  character  is  usually  associated  with  cases  of 
severe  infection  such  as  are  encountered  among  habitual  drunkards. 

Rarely  the  sputum  shows  no  evidence  of  blood  throughout  the  attack 
and  still  more  rarely  the  sputum  may  be  absent.  The  latter  is  apt  to  be 
the  case  in  children  who  swallow  the  sputum  and  in  delirious  or  stuporous 
patients  who  fail  to  cough  it  up.  While  the  expectoration  of  pure  blood 
may  occur  in  pneumonia,  the  occurrence  of  a  frank  hemoptysis  should 
arouse  one's  suspicions  as  to  the  possibility  of  a  tuberculous  rather  than  a 
pneumococcus  infection. 

Microscopically  the  sputum  shows  in  the  early  stages  the  presence 
of  crenated  red  blood  cells;  later  leukocytes,  shreds  of  fibrin  and  at  times 
Curschmann  spirals  and  casts  from  the  smaller  bronchioles.  The  type 
of  organism  has  been  dealt  with  under  the  section  on  bacteriology. 

Nervous  Symptoms. — As  an  initial  symptom  headache  is  common. 
In  children  the  attack  is  not  infrequently  ushered  in  with  a  convulsion. 
During  the  course  of  the  disease  delirium  is  apt  to  occur.  The  character 
of  the  delirium  varies  greatly;  in  some  instances  it  consists  of  slight  in- 
coherence; in  others,  especially  in  asthenic  and  senile  patients,  it  is 
commonly  of  the  stuporous  and  muttering  variety;  in  still  others  the 
delirium  takes  the  form  of  violent  maniacal  excitement  often  with  homi- 
cidal tendencies.  As  the  last-mentioned  condition  may  develop  suddenly 
pneumonia  patients  should  always  be  carefully  watched. 

Among  those  addicted  to  the  excessive  use  of  alcohol  the  occurrence 
of  delirium  resembling  delirium  tremens  is  not  uncommon.  Apex 
pneumonias  are  said  to  develop  a  severe  form  of  delirium  more  often 
than  those  with  a  lesion  at  the  base  of  the  lung.  Among  762-4  cases  of 
pneumonia  delirium  was  noted  in  1343  or  17  per  cent.  (Musser  and 
X orris). 

The  Blood. — There  is  no  anemia  which  can  be  ascribed  to  the  pneu- 
monia and  the  red  cells  and  hemoglobin  show  little  or  no  change.     There 


404      DISEASES   OF  THE  BRONCHI,   LUNGS,   PLEURA,   AND    DIAPHRAGM 

is,  however,  in  the  great  majority  of  cases  a  leukocytosis.  In  the  average 
case  the  white  cell  count  ranges  between  15,000  and  30,000;  it  may  be  as 
high  as  100,000.  Very  high  counts  are  often  associated  with  cases  of 
severe  infection  and  are  apt  to  terminate  fatally.  The  absence  of 
leukocytosis  is  a  bad  sign  and  often  points  to  an  unusually  severe 
infection  or  lack  of  resistance. 

The  Urine. — In  practically  all  cases  the  quantity  of  urine  is  greatly 
reduced,  highly  colored,  increased  in  specific  gravity  and  markedly  acid — 
the  so-called  febrile  urine.  Traces  of  albumen  are  usually  present  and 
there  may  be  tube  casts.  The  chlorides  are  greatly  diminished  or  entirely 
absent. 

Digestive  Symptoms. — In  children  the  onset  may  be  attended  with 
vomiting.  The  tongue  is  coated  with  a  white  fur  and  in  toxic  cases  it 
may  become  very  dry.  The  appetite  is  poor  and  the  bowels  usually 
constipated.  Diarrhea  may  arise  if  the  mucous  membrane  of  the  bowel 
becomes  the  seat  of  a  croupous  exudate.  A  very  troublesome  and  often 
dangerous  symptom  is  meteorism. 

The  Skin. — Labial  herpes  occur  so  frequently  in  croupous  pneumonia 
that  their  occurrence  is  always  of  diagnostic  value.  The  vesicles  may 
appear  at  the  angles  of  the  mouth  and  about  the  chin  or  nose.  Occasion- 
ally they  occur  about  the  genitals  and  anus.  The  frequency  of  herpes 
varies  greatly,  the  figures  ranging  from  5  to  50  per  cent.  Cases  in  which 
herpes  occur  are  said  to  have  a  better  prognosis. 

Sweating  may  occur  during  the  course  of  the  disease  but  as  a  rule  is 
noted  only  at  the  time  of  the  crisis  when  it  may  be  profuse.  Flushing 
of  the  cheek  on  the  affected  side  is  a  common  phenomenon. 

The  Crisis. — The  phenomena  which  characterize  the  crisis  or  termina- 
tion of  an  attack  of  lobar  pneumonia  constitute  the  most  remarkable 
feature  of  this  or  any  other  disease.  In  the  course  of  a  few  hours  a 
patient  who  has  been  desperately  ill  and  whose  fate  hangs  in  the  balance 
wakes  from  a  sound  sleep  nearly  free  from  his  distressing  symptoms;  and 
not  less  remarkable  is  the  fact  that  with  the  extraordinary  change  in 
the  subjective  symptoms  the  physical  signs  over  the  affected  lung 
remain  unaltered.  The  cause  of  this  sudden  change  is  believed  to  be 
due  to  the  establishment  of  an  active  immunity  to  the  toxin  of  the 
pneumococcus. 

As  already  stated  the  crisis  ,may  be  expected  on  or  about  the  seventh 
day  of  the  disease;  in  some  instances  it  occurs  a  clay  or  so  earlier  and  in 
others  it  is  delayed  for  several  days  longer. 

The  onset  of  the  crisis  may  be  heralded  by  a  disappearance  of  the 
restlessness  and  delirium;  the  flushed  face  becomes  pale;  and  the  anxious 
facial  expression  is  replaced  by  one  of  calm.  At  the  same  time  the  patient 
becomes  drowsy  and  falls  asleep.  The  sleep  at  first  broken  gradually 
deepens  and  may  last  from  5  to  12  hours  or  more.  During  this  time  the 
temperature  rapidly  falls  from  104°  or  105°F.  to  97°  or  98°F.  and  is 
accompanied  by  sweating  which  is  often  most  profuse.  In  some  instances 
the  temperature  may  fall  six  or  eight  degrees  within  1  hour,  while  in 
others  the  decline  lasts  as  long  as  24  hours.  The  temperature  may  show 
a  slight  rise  on  the  following  day  and  then  drop  permanently.  The 
respirations  become  slower,  the  pulse  rate  drops  and  the  cough  becomes 
looser  (see  Fig.  273).  The  rusty  character  of  the  sputum  may  persist 
for  a  few  days.     If  delirium  has  been  a  marked  feature  it  may  be  several 


DISEASES    OF    THE    LUNGS  405 

days  before  the  mind  is  entirely  clear.  In  a  case  free  from  complications 
the  convalescence  is  rapid,  recovery  being  usually  completed  in  about 
three  weeks. 

The  phenomena  just  described  occur  in  about  half  the  cases  terminat- 
ing favorably.  In  the  remainder  the  fever  instead  of  suddenly  disappear- 
ing gradually  subsides  by  lysis  and  at  the  same  time  there  is  a  gradual 
rather  than  a  rapid  abatement  of  the  symptoms.  The  more  prolonged 
the  attack  the  more  apt  is  the  termination  to  be  by  lysis. 

Physical  Signs. — The  following  description  is  that  of  frank  lobar 
pneumonia  as  it  occurs  in  the  adult.  The  commoner  variations  which 
characterize  the  atypical  case  will  be  considered  separately.  The  phys- 
ical signs  indicative  of  the  disease  manifest  themselves  in  from  24  to  48 
hours.  If  delayed  beyond  this  period,  it  is  usually  due  to  the  fact  that 
the  pneumonia  starts  in  the  central  portion  of  the  lung  and  gradually 
extends  toward  the  periphery.  In  some  instances  the  lesion  does  not 
extend  beyond  the  central  portion  of  the  lung  and  physical  signs  may  be 
absent  throughout  the  entire  course  of  the  disease. 

Inspection. — There  are  certain  striking  features  about  pneumonia 
even  from  its  onset,  that  render  the  probability  of  its  presence  apparent 
from  inspection  alone.  The  breathing  is  rapid  and  the  respirations  are 
short  and  shallow,  often  accompanied  by  an  "expiratory  grunt,"  inspira- 
tory dilatation  of  the  alse  nasi  and  an  exaggerated  action  of  the  accessory 
muscles  of  respiration,  such  as  the  sternocleidomastoids  and  scaleni. 
The  presence  of  herpes  labialis  is  very  suggestive.  One  cheek  may  be 
more  flushed  than  its  fellow  and  very  often  the  pupils  are  unequal,  the 
dilated  pupil  being,  as  a  rule,  on  the  affected  side. 

The  patient  usually  lies  flat  on  his  back  but  may  lie  on  the  affected 
or  unaffected  side.  In  the  effort  to  minimize  the  pain  the  patient  may 
be  propped  up  in  bed  and  inclined  toward  the  affected  side. 

Inspection  of  the  chest  itself,  especially  when  the  disease  is  fully 
developed,  will  show  a  diminution  of  expansion  on  the  affected  side  and 
an  exaggerated  movement  on  the  opposite  side.  When  the  lower  lobe  is 
affected  the  expansion  of  the  chest  over  the  upper  lobe  on  the  affected 
side  may  be  exaggerated.  Occasionally  when  the  left  lung  is  the  seat 
of  disease  the  involved  portion  may  pulsate  synchronously  with  the  heart. 
Inspection  of  the  cardiac  area  shows  nothing  abnormal. 

Palpation. — Diminished  expansion  of  one  side  as  compared  to  the 
other  may  be  more  apparent  from  palpation  than  inspection.  During 
the  stage  of  engorgement  which  usually  lasts  from  12  to  24  hours  the 
tactile  fremitus  may  show  no  change  but  during  the  period  of  consolida- 
tion it  is  exaggerated.  Absent  or  diminished  expansion  occurs  in  cases 
of  central  pneumonia  and  in  the  so-called  massive  pneumonia  when  the 
bronchi  are  plugged  with  the  fibrinous  exudate.  Occasionally  a  friction 
or  rhonchial  fremitus  may  be  felt.  Pressure  over  the  consolidated  area 
will  often  elicit  a  tender  spot,  the  pain  being  referred  to  a  point  some 
distance  away. 

The  pulse  in  sthenic  lobar  pneumonia  is  full  and  bounding  once  the 
disease  has  become  established.  During  the  chill  it  is  small  and  in  the 
aged  or  debilitated  it  may  be  weak  and  rapid  throughout. 

Formerly  considerable  emphasis  was  placed  on  the  pulse-respiration 
ratio.  In  health  this  is  about  4.5  to  1,  while  in  pneumonia  it  maybe  3  to 
1,  2  to  1,  or  even  1  to  1.     In  an  obscure  case  this  ratio  is  suggestive  of 


406      DISEASES   OF  THE  BRONCHI,   LUNGS,   PLEURA,   AND   DIAPHRAGM 

pneumonia  as  there  is  ;io  other  febrile  disease  in  which  the  respirations 
are  so  frequently  increased  out  of  proportion  to  the  pulse. 

In  the  case  of  average  severity  the  pulse  ranges  from  100  to  110. 
Generally  speaking  a  low  pulse  rate  is  a  favorable  indication.  When 
the  rate  is  120  or  over  the  outlook  is  serious,  as  it  has  long  been  noted 
that  a  high  pulse  rate  is  attended  by  a  very  high  mortality.  The  pulse 
rate  in  women  tends  to  be  slightly  higher  than  in  men.  A  high  pulse 
rate  in  children  does  not  have  the  same  significance  as  in  adults  as  the 
former  not  uncommonly  have  a  rate  ranging  from  120  to  150.  Irregu- 
larity of  the  pulse  is  also  to  be  viewed  as  a  very  serious  symptom.  Of 
17  patients  with  an  irregular  pulse  13  died  (Lord). 

A  few  years  ago  G.  A.  Gibson  pointed  out  that  when  the  blood-pressure 
as  expressed  in  millimeters  of  mercury  does  not  fall  below  the  pulse  rate 
as  expressed  in  beats  per  minute,  the  patient  is  in  no  immediate  danger. 
With,  for  example,  a  pulse  rate  of  100  and  a  blood-pressure  of  125  there 
is  no  need  for  interference  but  if  this  ratio  becomes  reversed  active 
stimulation  is  demanded  in  order  to  relieve  the  threatened  cardiac 
failure.  While  this  observation  is  of  importance  it  is  not  to  be  depended 
on  absolutely. 

Percussion. — The  percussion  note  over  the  affected  lobe  may,  if  the 
case  is  seen  early,  be  tympanitic  in  quality.  As  the  consolidation  in- 
creases the  note  becomes  absolutely  dull  and  there  is  in  addition,  a  feeling 
of  resistance.  The  dull  note  remains  even  after  the  crisis  but  with  the 
onset  of  resolution  the  note  gradually  becomes  more  and  more  resonant. 
Occasionally  the  note  may  become  resonant  within  two  or  three  days  but 
as  a  rule  several  weeks  elapse  before  the  normal  standard  has  been  re- 
gained. Very  often  in  percussing  over  the  affected  area  varying  degrees 
of  hypersensitiveness  are  encountered  due  to  the  associated  pleurisy. 
If  the  lesion  is  situated  some  distance  from  the  periphery  of  the  lung  the 
note  will  show  little  if  any  impairment  and  may  even  be  hyperresonant. 
Over  the  unaffected  portions  the  note  is  resonant  or  if  the  consolidation 
is  extensive  the  note  may  be  hyperresonant  as  the  result  of  compensatory 
emphysema. 

Auscultation.— At  the  onset  of  the  disease  the  breath  sounds  over  the 
affected  area  may  be  slightly  suppressed  or  even  harsher  than  normal, 
and  broncho-vesicular  in  character;  usually  they  are  somewhat  sup- 
pressed. The  ?nost  important  diagnostic  sign  during  the  first  stage  is  the 
crepitant  rale. 

The  distinctive  features  of  crepitant  rales  are  that  they  produce  a 
fine,  crackling,  high-pitched,  sound,  which  occurs  abruptly  at  the  end 
of  inspiration,  especially  a  forced  inspiration;  they  are  never  heard  dur- 
ing expiration.  The  resemblance  between  the  sound  produced  by  a 
shower  of  crepitant  rales  and  that  by  rubbing  the  hair  between  the  fingers 
close  to  the  ear  is  so  similar  as  to  make  the  comparison  a  very  apt  one. 
The  crepitant  rale  is  heard  during  the  first  day  or  so  only. 

The  crepitant  rale  while  a  very  important  diagnostic  sign  in  lobar 
pneumonia  is  not  absolutely  pathognomic  as  it  may  occur  in  a  localized 
area  at  the  apex  as  an  accessory  sign  of  phthisis.  It  occurs  transiently 
under  the  following  circumstances :  A  patient  who  has  been  confined  for 
some  time  in  bed,  lying  on  the  back  and  much  enfeebled  with  any  dis- 
ease, if  suddenlv  raised  to  a  sitting  posture  and  auscultated,  a  crepitant 
rale  is  often  found  on  the  posterior  aspect  of  the  chest  at  the  end  of  forced 


DISEASES    OF    THE    LUNGS  407 

inspiration.  The  rale  disappears  after  a  few  forced  inspirations  and  is 
heard,  not  on  one  side  only,  but  on  both  sides.  It  should  be  mentioned 
also  that  if  the  stethoscope  be  applied  to  a  hairy  chest  the  movements 
in  the  act  of  inspiration  may  produce  a  sound  identical  with  the  crepi- 
tant rale  (Flint). 

When  the  vesicles  become  entirely  filled  with  the  exudate  and  the 
lung  presents  a  solid  appearance  no  extraneous  sounds  are  produced. 
When  this  stage  is  reached  the  breath  sounds  become  tubular  or  bronchial 
in  character,  the  inspiration  being  high-pitched  and  of  the  same  duration 
as  expiration.  In  the  ordinary  case  of  frank  pneumonia  the  bronchial 
breathing  is  usually  quite  loud.  The  voice  sounds  are  also  intensified 
and  exaggeration  of  the  spoken  voice  and  bronchophony  are  usually 
marked.  The  whispered  voice  is  also  distinctly  transmitted.  Both 
•the  spoken  and  whispered  voice  may  have,  at  times,  the  peculiar  quality 
known  as  segophony.  This  sign  is  common  in  cases  of  pleural  effusion 
but  it  may  also  occur  over  consolidated  lung  tissue.  In  cases  of  massive 
pneumonia  both  the  breath  and  voice  sounds  may  be  very  distant  or 
entirely  absent.  Over  the  unaffected  portions  of  the  lungs  the  breath 
sounds  are  clear  and  slightly  exaggerated  but  in  those  cases  in  which 
an  attack  of  bronchitis  has  preceded  the  pneumonia  rales  may  be  present. 

In  examining  the  chest  of  an  individual  suspected  of  having  pneu- 
monia care  should  be  taken  not  to  overlook  the  axillary  region.  Very 
often  when  the  pneumonia  affects  the  upper  lobe  physical  signs  will  be 
obtained  only  high  up  in  the  axilla. 

With  the  onset  of  gray  hepatization  rales  are  again  heard.  The  return- 
ing rale  or  crepitus  redux,  is  held  by  some  to  be  identical  with  the  crepi- 
tant rale  of  the  first  stage,  but  others  consider  it  coarser  and  lacking  the 
distinctive  features  of  the  latter.  In  addition  to  the  crepitus  redux  there 
are  to  be  heard  numerous  subcrepitant  rales.  As  the  vesicles  are  emptied 
of  their  contents  the  character  of  the  breath  sounds  gradually  change; 
the  bronchial  breathing  becomes  broncho-vesicular  in  character  and 
finally  pure  vesicular,  although  for  a  time  the  vesicular  murmur  is  apt 
to  be  less  intense.  The  restoration  of  the  breath  sounds  to  the  normal 
may  occur  rapidly  but,  as  a  rule,  weeks  elapse  before  this  is  attained. 

Careful  examination  of  the  heart  should  be  a  routine  procedure  in 
cases  of  lobar  pneumonia.  Early  in  the  disease  the  heart  sounds  usually 
show  no  change  unless  toxic  symptoms  are  marked  from  the  onset.  In 
the  later  stages  of  the  attack  functional  murmurs  are  very  common.  In 
a  few  cases  the  murmur  will  be  due  to  an  acute  endocarditis  and,  as  has 
been  shown  in  the  section  on  morbid  anatomy,  this  is  not  uncommonly 
ulcerative  in  character.  The  second  pulmonic  sound  is  generally  accentu- 
ated and  may  be  reduplicated  as  well.  A  diminution  of  the  accentuation 
of  the  pulmonic  second  sound  is  to  be  regarded  seriously  as  it  is  often  a 
forerunner  of  acute  dilatation  of  the  right  ventricle.  Cardiac  failure  may 
manifest  itself  by  sudden  syncope  but  more  often  it  develops  more  or 
less  gradually.  The  pulse  becomes  more  rapid  and  in  addition  there 
arc  cyanosis,  dyspnea  and  cold  extremities.  The  above  symptoms  may 
occur  at  or  about  the  time  of  the  crisis;  occurring  at  this  time  they  are, 
as  a  rule,  often  mild  and  of  brief  duration.  Occurring  after  crisis  even 
mild  symptoms  of  cardiac  failure  are  serious  as  they  indicate  consider- 
able damage  of  the  heart  muscle.  Cardiac  weakness  develops  as  a,  rule, 
in  cases  with  severe  toxemia,  extensive  consolidation  and  hyperpyrexia. 


408       DISEASES   OF   THE  BRONCHI,    LUNGS,    PLEURA,    AND   DIAPHRAGM 

We  have  already  alluded  to  the  high  incidence  of  pericarditis  in  the 
post-mortem  room  as  compared  to  the  clinical  findings.  While  a  more 
careful  examination  of  the  precordium  would  undoubtedly  bring  about 
a  higher  percentage  of  cases  of  clinical  pericarditis,  it  is  to  be  borne  in 
mind  that  the  pericardial  changes  are  often  terminal  in  character  and 
furthermore,  that  the  confusion  of  sounds  often  renders  an  accurate 
observation  very  uncertain. 

In  a  study  of  the  physical  signs  occurring  in  the  early  stages  of  pneu- 
monia Conner  and  Dodge  determined  their  frequency  as  follows:  (1) 
Circumscribed  area  of  feeble  and  indistinct  breathing  as  compared  with 
the  opposite  side.  (2)  Circumscribed  impairment  without  or  with  tym- 
panitic quality  (sitting  up).  (3)  Crepitant  rales.  (4)  Slight  increase  in 
intensity  and  clearness  of  vocal  resonance. 

Wilson  Fox  gives  the  following  sequence  of  physical  signs,  corre- 
sponding to  the  anatomical  stages  of  engorgement,  hepatization,  and 
resolution. 

1.  Altered  characters  of  the  respiratory  sound,  which  may  be  weaker 
or  harsher  than  natural,  and  attended  or  immediately  followed  by  fine, 
crackling  rales. 

2.  Dulness  on  percussion,  attended  by  bronchial  or  tubular  or  sup- 
pressed breathing,  bronchophony  and  increased  vocal  fremitus,  together 
with  diminished  respiratory  movement,  chiefly  affecting  the  act  of 
expansion. 

3.  The  return  of  crepitation,  usually  in  a  coarser  form;  gradual 
diminution  of  percussion  dulness,  together  with  the  return  of  the  respira- 
tory movements  and  of  the  characters  of  the  respiration  and  of  the  vocal 
resonance  and  fremitus  to  the  healthy  standard. 

The  Stage  of  Resolution. — The  duration  of  this  stage  varies  greatly. 
Rarely  there  may  be  a  restoration  to  the  normal  within  two  or  three 
days  after  the  crisis.  In  the  great  majority  of  cases  three  or  four  weeks 
or  even  longer  must  elapse  before  physical  signs  indicating  a  normal 
lung  are  obtained.  In  a  series  of  40  cases  in  which  resolution  was  unduly 
delayed  McCrae  found  that  the  duration  extended  to  the  fourth  week 
in  5  cases,  fifth  week  in  10  cases,  sixth  week  in  4  cases,  ninth  week  in  3 
cases,  and  tenth,  eleventh  and  twelfth  weeks  each  1  case.  The  gradual 
disappearance  of  the  consolidated  area  can  be  observed  from  day  to  day. 
If  no  such  change  is  apparent  one  should  be  alert  to  the  possibility  of 
an  abscess,  gangrene  or  the  development  of  an  effusion.  The  former 
two  conditions  will  generally  manifest  themselves  sooner  or  later,  by 
typical  symptoms.  The  presence  of  an  effusion  is  more  apt  to  be  over- 
looked. One  not  infrequently  sees  cases  in  which  it  is  stated  that 
resolution  has  never  taken  place  and  that  the  signs  of  consolidation 
persist.  As  a  rule  one  of  two  things  has  occurred:  either  the  pneumonia 
has  been  complicated  by  an  effusion  or,  as  occasionally  happens,  an 
attack  of  dry  pleurisy,  followed  by  an  effusion,  was  ushered  in  with  chilly 
sensations,  fever  and  pain  in  the  side  thus  simulating  lobar  pneumonia. 
Rarely  the  affected  portion  gradually  undergoes  fibroid  changes.  Absorp- 
tion of  the  exudate  and  the  restoration  of  the  lung  to  its  normal  state  is 
the  rule ;  therefore  in  any  case  in  which  the  physical  signs  show  no  change 
one  should  always  bear  in  mind  the  possibility  of  one  of  the  above  changes 
being  present  and  by  means  of  an  explorihg  needle  and  the  X-rays  deter- 
mine the  exact  nature. 


DISEASES    OF    THE    LUNGS  409 

Relapse. — There  is  considerable  confusion  as  to  the  meaning  of  this 
term.  Its  use  should  be  restricted  to  those  rare  instances  in  which  a  few 
days  after  the  subsidence  of  the  original  attack  a  fresh  invasion  of  the 
lung  tissue  occurs.  "If  the  lung,  after  an  ordinary  croupous  pneumonia 
involving  one  or  several  lobes,  becomes  normal  after  the  fever  has  termi- 
nated by  crisis  or  lysis,  the  patient  is  convalescent;  and  if  at  least  three 
days  or  several  weeks  after  the  deferescence  a  new  infiltration  of  the  same 
or  other  lobes  with  all  the  characteristic  phenomena  of  a  local  and  general 
nature  occur,  a  relapse  has  without  question  taken  place"   (Wagner). 

Among  5966  cases  collected  from  the  literature  a  relapse  occurred  in 
36  or  0.60  per  cent.  (Norris). 

Clinical  Varieties  of  Pneumonia. — Pneumonia  is  not  infrequently 
encountered  in  forms  which  present  more  or  less  well-marked  variations 
from  the  ordinary  frank  type  of  the  disease.  In  some  instances  nothing- 
more  is  meant  than  that  certain  symptoms  predominate;  in  others  the 
variation  has  reference  to  the  character  of  the  anatomical  lesion. 

Asthenic  Pneumonia. — This  term  is  applied  to  pneumonias  character- 
ized by  extreme  prostration.  The  onset  is  often  insidious.  Physical 
signs  may  be  absent  and  this  is  also  true  of  the  subjective  symptoms. 
In  other  instances  there  are  severe  nervous  symptoms  such  as  delirium, 
great  prostration  and  finally  coma.  Asthenic  pneumonia  is  a  common 
occurrence  in  the  aged  and  in  those  enfeebled  by  chronic  illness. 

Senile  Pneumonia. — This  is  essentially  the  same  as  asthenic  pneu- 
monia. The  disease  as  seen  in  those  of  advanced  years  very  commonly 
has  an  insidious  onset,  ill-defined  physical  signs  and  severe  constitutional 
symptoms. 

Terminal  Pneumonia. — In  those  who  are  the  victims  of  some  chronic 
affection  such  as  diabetes,  cardiac,  renal  or  pulmonary  disease  the  final 
act  of  the  drama  may  be  an  attack  of  pneumonia.  Terminal  pneumonias 
are  common  during  the  winter  months  and  like  the  asthenic  and  senile 
types  are  often  characterized  by  a  paucity  of  physical  signs  and  marked 
prostration. 

The  three  types  above  mentioned  are  not  infrequently  overlooked 
because  they  lack  the  characteristic'  features  of  frank  pneumonia  both 
as  regards  the  physical  signs  and  the  symptoms.  The  occurrence  of 
respiratory  symptoms  no  matter  how  slight  or  evidences  of  prostration  in 
the  aged  and  in  those  suffering  from  some  chronic  ailment  should  always 
suggest  the  possibility  of  lobar  pneumonia. 

Pneumonia  in  Alcoholic  Subjects. — In  this  type  the  cerebral  symptoms 
are  frequently  so  marked  as  to  suggest  delirium  tremens.  The  respira- 
tory symptoms  may  be  very  trivial.  It  is  currently  believed  that  in 
alcoholics  the  disease  affects  the  apex  of  the  lung  more  frequently  than 
the  base. 

Typhoid  Pneumonia. — Mention  is  made  of  this  term  simply  to  cau- 
tion against  its  use.  The  designation  is  misleading  as  one  is  never 
certain  whether  it  has  reference  to  a  patient  who  has  passed  into  the 
typhoid  state  or  whether  the  pneumonia  has  been  associated  with 
typhoid  fever. 

Larval  or  Abortive  Pneumonia. — Occasionally  cases  are  seen  in  which 
the  disease  runs  a  course  of  from  one  to  three  days.  In  such  cases  the 
symptoms  may  be  quite  characteristic  of  pneumonia  but  the  physical 
findings  are,  as  a  rule,  inconclusive.     Abortive  pneumonia  is  most  apt 


410       DISEASES    OF   THE  BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

to  be  encountered  in  institutions  in  which  the  disease  is  for  the  time 
prevailing. 

Epidemic  Pneumonia. — The  fact  that  pneumonia  may  assume  the 
portions  of  a  mild  epidemic  has  already  been  alluded  to  in  dealing  with 
the  etiology  of  the  disease. 

Post-operative  pneumonia  has  been  referred  to  under  etiology. 

Central  Pneumonia. — In  those  cases  in  which  the  symptoms  point 
conclusively  to  lobar  pneumonia  but  in  which  physical  signs  are  very 
slight  or  wanting,  the  lesion  is  deep-seated  or  centrally  placed.  This 
may  continue  throughout  the  disease  or  after  three  or  four  clays  the 
lesion  may  extend  sufficiently  near  the  periphery  of  the  lung  to  admit 
of  its  recognition. 

Apex  Pneumonia. — When  lobar  pneumonia  affects  the  upper  lobes 
it  is  believed  to  be  of  a  more  severe  type.  Prostration,  hyperpyrexia, 
and  cerebral  symptoms  are  often  marked.  In  children  and  in  alcoholics 
the  apex  is  very  commonly  involved.  The  right  apex  is  affected  about 
twice  as  often  as  the  left. 

Wandering  or  Creeping  Pneumonia. — Practically  every  case  of  pneu- 
monia spreads  to  some  extent.  As  a  rule,  it  extends  from  a  given  spot 
but  limits  itself  sharply  to  one  lobe.  In  some  cases,  however,  it  slowly 
extends  spreading  from  lobe  to  lobe  by  contiguity;  in  others  the  process 
apparently  develops  afresh  at  different  points  in  the  same  or  even  the 
opposite  lung. 

Massive  Pneumonia. — -This  is  a  rare  form  in  which  the  large  bronchi 
become  entirely  filled  with  the  croupous  exudate.  Owing  to  the  block- 
ing of  the  bronchi  the  physical  signs  may  be  limited  to  marked  flatness 
on  percussion  such  as  occur  in  pleurisy  with  effusion.  Both  the  breath 
and  voice  sounds  are  absent. 

Double  Pneumonia. — Both  bases  may  be  affected  simultaneously  or 
the  apex  of  one  lung  and  the  lower  lobe  of  the  opposite  lung  may  be 
involved. 

Pneumonia  in  Children. — Lobar  pneumonia  as  seen  in  young  children 
often  presents  well-marked  differences  from  the  disease  as  it  occurs  in 
adults.  Instead  of  the  initial  chill  the  disease  may  be  ushered  in  with 
an  attack  of  vomiting,  occasionally  by  a  convulsion,  or  the  child  may  be 
listless  and  refuse  to  eat  for  several  clays  prior  to  the  onset  of  the  fever. 
The.  temperature  rises  rapidly  and  is  usually  higher  than  that  seen  in 
adults,  often  reaching  105°  to  107°F.  Nervous  symptoms  are  usually 
prominent,  the  child  becoming  delirious  and  unable  to  recognize  anyone; 
later  the  delirium  is  succeeded  by  drowsiness  and  semiconsciousness. 
Vomiting  which  may  be  severe  and  persistent  is  often  a  marked  feature 
of  the  disease  in  children.  These  symptoms  at  first  sight  suggest  some 
cerebral  affection  especially  meningitis  but  meningitis  rarely  has  so  acute 
an  onset. 

Occasionally  a  child  ill  with  pneumonia  develops  an  erythematous 
rash  which  bears  a  superficial  resemblance  to  scarlet  fever.  It  differs 
from  the  rash  associated  with  the  latter  in  that  it  is  not  punctate  and  is 
of  brief  duration. 

The  disturbance  of  the  pulse  respiration  ratio  (normally  4.5  to  1) 
is  very  suggestive.  Expectoration  is  rare  in  children  as  they  usually 
swallow  the  sputum. 

The  apex  of  the  lung  is  affected  somewhat  more  frequently  than  the 


DISEASES    OF    THE    LUNGS  411 

lower  lobe.  The  physical  signs  may  for  a  few  clays  be  entirely  absent  or 
very  inconclusive.  Northrup  has  epitomized  the  physical  findings  as 
follows:  Absent  or  diminished  respiratory  murmur  over  one  lobe  or 
.portion  of  a  lobe;  rales  of  any  kind,  perhaps  appearing  only  late,  either 
in  a  localized  shower  or  diffusely  scattered ;  broncho-vesicular  breathing — 
a  bronchial  whiff;  slight  dulness,  becoming  marked  only  late;  and,  lastly, 
cough. 

Mason1  in  a  study  of  the  X-ray  findings  in  lobar  pneumonia  in  young 
children  found  that  the  consolidated  area  was  triangular  or  conical  in 
shape  with  the  base  at  the  periphery  of  the  lung.  The  consolidation 
always  started  at  the  periphery  and  extended  in  toward  the  hilus,  and 
the  base  of  the  consolidated  area  is  very  frequently  situated  at  a  point 
corresponding  to  the  apex  of  the  axilla.  It  is  well  known  that  lobar 
pneumonia  as  it  occurs  in  children  may  be  attended  with  nothing  more 
than  slight  impairment  of  the  percussion  note,  bronchial  breathing  and 
voice  being  absent.  In  the  absence  of  the  latter  signs  Mason  states 
that  the  pneumonic  process  does  not  extend  to  the  hilus.  This  leaves 
an  area  of  normal  air  tissue  which  dissipates  the  bronchial  quality  of  the 
breath  and  voice  sounds  which  have  their  origin  in  the  trachea  and  large 
bronchi  at  the  root  of  the  lung.  Absent  or  slight  physical  signs  are  due 
therefore  to  peripheral  rather  than  a  central  location  of  the  pneumonic 
process. 

Secondary  Pneumonia. — This  form  is  met  with  chiefly  as  a  complica- 
tion of  one  of  the  specific  fevers  particularly  diphtheria,  typhoid  fever, 
typhus  and  influenza.  The  symptoms  are  often  indefinite  and  the 
physical  signs  of  equivocal  import.  The  symptoms  are  apt  to  lack  the 
striking  features  of  frank  croupous  pneumonia  and  the  physical  signs 
rarely  amount  to  more  than  impaired  resonance,  feeble  breathing  and 
a  few  crackling  rales.  One  is  often  in  doubt  as  to  whether  there  is  a 
hypostatic  congestion,  edema,  pulmonary  infarct,  a  central  pneumonia 
or  a  broncho-pneumonia. 

A  disturbance  of  the  normal  pulse-respiration  ratio — 4.5  to  1 — is 
always  suggestive  and  should  lead  to  careful  physical  examination. 
In  spite  of  precautions  the  lesion  is  often  overlooked. 

Diagnosis  of  Pneumonia. — The  recognition  of  a  typical  case  of  pneu- 
monia is  in  the  great  majority  of  instances,  an  easy  matter.  A  history 
of  a  chill  followed  by  pain  in  the  side,  fever,  rapid  respirations,  the 
presence  of  herpes,  a  leukocytosis  and  bloody  or  rusty  sputum  are  of 
themselves  sufficient  to  warrant  a  diagnosis,  even  in  the  absence  of  phys- 
ical signs.  The  latter  it  is  to  be  recalled,  may  not  be  present  for  a  few 
days  and  in  some  cases  are  never  definitely  determined.  When  present 
the  physical  signs  taken  in  conjunction  with  the  symptoms  render  the 
diagnosis  practically  certain.  The  evolution  of  the  physical  signs  has 
been  considered  in  full  and  need  not  be  considered  further. 

In  the  great  majority  of  cases  of  atypical  pneumonia  the  disease  occurs 
in  the  aged,  in  those  debilitated  by  some  chronic  disease  and  in  children. 
In  such  cases,  while  the  patient  is  usually  very  ill,  there  is  a  paucity  of 
both  physical  signs  or  symptoms  or  the  symptoms  while  very  severe  arc 
not  such  as  occur  in  typical  pneumonia.  One  should  always  recall  that 
under  these  circumstances  pneumonia  is  always  a  possibility  and  every 
means  should  be  taken  to  determine  its  presence.  It  is  in  such  cases  that 
1  Amer.  Jour.  Diseases  of  Children,  March,  1916. 


412      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

alterations  in  the  pulse-respiration  ratio  sometimes  furnish  the  clue. 
A  leukocytosis  also  points  to  pneumonia  although  in  very  severe  cases 
a  leukopenia  may  be  present.  If  expert  laboratory  assistance  is  avail- 
able, a  blood  culture  should  be  made  in  doubtful  cases  as  this  is  the  most 
certain  method  we  possess. 

The  conditions  which  are  most  likely  to  be  confused  with  lobar  pneu- 
monia are  acute  tuberculous  pneumonia  or  pneumonic  phthisis,  broncho- 
pneumonia, pleural  effusion,  pulmonary  congestion,  pulmonary  infarct 
and  atelectasis. 

Acute  Tuberculous  Pneumonia. — Acute  pneumonic  phthisis  is  con- 
sidered in  full  in  the  section  dealing  with  tuberculosis.  It  is  sufficient 
to  remark  here  that  tuberculosis  often  first  manifests  itself  with  a  chill, 
pain,  cough  and  signs  of  consolidation.  In  some  instances  it  is  impossible 
for  a  week  or  more  to  distinguish  it  from  lobar  pneumonia.  At  the  end 
of  ten  days  or  two  weeks,  however,  the  temperature  changes  from  the 
continuous  to  the  remittent  or  intermittent  type  and  the  sputum  becomes 
purulent  in  character.  While  pure  bronchial  breathing  may  be  heard 
over  the  consolidated  area  the  absence  of  breath  sounds  is  not  unusual 
and  is  of  considerable  diagnostic  importance.  In  every  case  of  pro- 
tracted pneumonia  the  sputum  should  be  examined  for  tubercle  bacilli. 

Acute  tuberculous  pneumonia  usually  involves  one  of  the  upper  lobes 
and  in  the  majority  of  cases  occurs  in  an  individual  whose  health  has 
been  bad  or  who  has  had  previous  pulmonary  trouble.  The  occurrence 
of  an  hemoptysis  points  to  tuberculosis  rather  than  pneumonia. 

Rarely  true  lobar  pneumonia  occurs  in  a  definitely  tuberculous  in- 
dividual. A  young  woman  with  a  moderately  advanced  tuberculous 
lesion  at  the  right  apex  which  had  become  arrested,  was  suddenly  seized 
with  a  chill,  pain  in  the  right  side  and  cough.  The  temperature  rapidly 
rose  to  103°F.  and  the  respirations  to  30.  At  the  end  of  two  days  a 
small  area  of  dulness  and  bronchial  breathing  was  heard  near  the  angle 
of  the  scapula;  this  gradually  spread  and  involved  all  of  the  right  lower 
lobe.  The  attack  ran  a  course  of  two  weeks,  the  temperature  falling  by 
lysis.  In  the  course  of  the  next  three  months  the  lower  lobe  gradually 
was  restored  to  normal.  There  was  no  lighting  up  of  the  tuberculous 
process.  In  this  case  it  was  impossible  to  tell  during  the  attack  or  indeed 
for  some  weeks  afterward,  whether  the  process  was  a  true  pneumonia  or  a 
widespread  tuberculous  infiltration. 

Broncho-pneumonia. — There  is  no  difficulty  in  distinguishing  between 
typical  lobar  pneumonia  and  broncho-pneumonia  but  in  those  of  ad- 
vanced years  and  in  the  debilitated  croupous  pneumonia  not  infrequently 
is  mistaken  for  the  broncho-pneumonic  form.  The  principle  features  of 
broncho-pneumonia  are  a  gradual  onset  and  a  much  longer  duration 
than  occurs  in  lobar  pneumonia.  Dyspnea  and  cyanosis  are  more  marked 
than  in  the  lobar  form  and  the  temperature  is  lower  and  subject  to 
more  marked  intermissions.  Both  lungs  are  affected  and  the  physical 
examination  shows  a  preponderance  of  signs  of  bronchitis  over  those  of 
consolidation. 

Pleural  Effusion. — At  first  sight  the  distinction  between  a  pleural 
effusion  and  lobar  pneumonia  should  be  easy.  As  a  matter  of  fact  the 
mistaking  of  the  one  for  the  other  is  not  uncommon.  In  some  instances 
the  differentiation  is  not  easy  and  one  cannot  be  certain  without  having 
recourse  to  the  exploring  needle,  a  procedure  which  should  always  be 


DISEASES    OF    THE    LUNGS  413 

followed  in  doubtful  cases.  In  the  typical  case  of  pneumonia  there  is 
bronchial  breathing  and  increased  vocal  and  tactile  fremitus  while  in 
pleural  effusion  the  breath  sounds  are  absent  or  very  distant  and  the 
fremitus,  both  vocal  and  tactile,  is  absent.  It  not  infrequently  happens, 
however,  that  the  signs  peculiar  to  one  may  occur  in  the  other.  Thus 
distant,  almost  inaudible,  breath  sounds  may  occur  in  pneumonia  while 
over  an  effusion  loud  bronchial  breathing  may  be  heard.  iEgophony 
over  the  upper  limit  of  an  effusion  is  considered  peculiar  to  this  condition 
but  it  may  occur  over  consolidation  as  I  had  occasion  to  note  only  re- 
cently. In  large  effusions  which  fill  one-half  or  two-thirds  of  the  pleural 
cavity  little  difficult}'  is  experienced  as  the  bulging  of  the  affected  side, 
the  obliteration  of  the  interspaces,  the  lack  of  motion  and  the  displace- 
ment of  the  apex  beat  of  the  heart  renders  a  diagnosis  possible  in  most 
cases  by  inspection  alone.  It  is  the  small  effusion  in  which  displacement 
of  the  thoracic  viscera  does  not  occur,  that  makes  the  diagnosis  difficult. 
The  presence  or  absence  of  Grocco's  triangle  is  often  of  service.  The 
exploring  needle  or  X-rays  should  always  be  resorted  to  in  case  of  doubt. 

There  is  another  phase  of  the  subject  which  should  be  mentioned, 
namely,  the  development  of  an  effusion  in  association  with  the  pneumonic 
process.  As  a  rule  such  effusions  are  purulent  in  character;  in  children 
they  are  practically  always  so.  Generally  no  suspicion  arises  as  to 
their  presence  until  after  the  stage  of  resolution  has  set  in.  It  then  be- 
comes apparent  that  the  affected  lung  is  not  clearing  up  and  that  the 
physical  signs  persist.  The  diagnosis  rests  partly  on  symptoms  and 
partly  on  physical  signs.  If  the  temperature  has  fallen  by  crisis  there  is 
a  secondary  rise  two  or  three  days  later  and  the  respiratory  rate  either 
fails  to  fall  or  becomes  increased.  If  the  temperature  falls  by  lysis,  a 
secondary  rise  may  occur  before  the  normal  has  been  reached. 

There  may  be  absence  of  breath  sounds  but  as  the  fluid  has  formed 
over  consolidated  lung  the  breathing  may  be  bronchial.  If  the  effusion 
gradually  increases  in  size,  bulging,  lack  of  motion  and  displacement  of 
the  viscera  take  place.  It  is  to  be  borne  in  mind  that  an  empyema, 
sometimes  loculated,  is  not  infrequently  the  cause  of  symptoms  and  phys- 
ical signs  ascribed  to  delayed  resolution. 

Pulmonary  Congestion. — Very  often  patients  who  have  been  confined 
to  bed  because  of  some  protracted  illness  such  as  typhoid  fever,  develop 
varying  degrees  of  congestion  in  the  posterior  portions  of  the  lungs, 
especially  at  the  bases.  The  condition  is  always  bilateral.  The  breath- 
ing may  be  somewhat  suppressed  but  is  otherwise  normal  and  the  per- 
cussion note  is  rarely  more  than  slightly  impaired.  Very  often,  however, 
fine  crepitating  rales  are  heard  which  are  indistinguishable  from  those 
occurring  in  pneumonia.  Often  they  are  transient  and  disappear  after 
a  few  deep  breaths  but  they  may  persist.  The  fact  that  the  condition  is 
bilateral  and  the  knowledge  that  it  is  not  uncommon  in  those  long  con- 
fined to  bed  should  serve  to  distinguish  it  from  pneumonia. 

Pulmonary  Infarct. — -Among  those  suffering  from  chronic  valvular 
heart  disease  the  occurrence  of  a  pulmonary  infarct  is  not  uncommon. 
The  onset  is  abrupt,  due  to  plugging  of  one  of  the  pulmonary  vessels  by 
an  embolism.  The  patient  is  usually  seized  suddenly  with  pain  in  the 
side,  shortness  of  breath,  and  later  there  is  cough  and  the  expectoration 
of  bloody  sputum.  On  physical  examination  there  may  be  a  small  area 
of  crepitating  rales  with  or  without  dulncss  on  percussion  and  bronchial 


414      DISEASES   OF  THE  BRONCHI,   LUNGS,   PLEURA,   AND   DIAPHRAGM 

breathing.  In  some  instances  the  physical  signs  closely  resemble  those 
obtained  in  pleurisy  with  effusion.  The  temperature  is  usually  low. 
Fowler  states  that  in  cases  of  infarction  the  patient  will  almost  certainly 
be  found  sitting  up  in  bed  while  this  rarely  happens  in  pneumonia. 
Examination  of  the  heart  should  make  it  possible  to  determine  the  exist- 
ence of  a  valvular  lesion  if  this  is  not  known  already. 

Pulmonary  infarction  as  the  result  of  venous  thrombosis  is  more 
confusing  as  the  pulmonary  symptoms  may  appear  before  the  thrombosis 
in  the  vein  manifests  itself.  The  continuation,  day  after  clay,  of  frankly 
bloody  sputum  associated  with  physical  signs  of  consolidation  in  one  of 
the  lower  lobes  is  very  suggestive  of  pulmonary  infarction  due  to  a 
venous  thrombosis. 

Atelectasis  or  Collapse  of  the  Lung. — Collapse  of  one  of  the  lower  lobes 
of  the  lungs  may  be  mistaken  for  pneumonia.  The  condition  is  some- 
times seen  in  association  with  acute  bronchitis,  great  hypertrophy  of 
the  heart  or  in  large  pericardial  effusions.  Pasteur  has  called  attention 
to  massive  collapse  of  one  of  the  lower  lobes  following  surgical  operations. 

Collapse  of  one  of  the  pulmonary  lobes  may  occur  with  the  same 
suddenness  and  intensity  as  a  pulmonary  embolism,  but  in  most  instances 
it  is  attended  by  less  violent  symptoms.  The  condition  is  characterized 
by  dyspnea,  pain  in  the  chest  and  the  expectoration  of  viscid  sputum. 
Usually  the  symptoms  subside  rapidly,  rarely  lasting  more  than  24  hours. 
If  the  viscid  sputum  persists  for  a  longer  period  it  is  likely  that  a  bron- 
chitis or  broncho-pneumonia  has  developed  in  the  reexpancling  lung. 

Physical  examination  shows  some  retraction  of  the  affected  side, 
impairment  of  the  percussion  note,  weak,  tubular  breathing,  and  the 
absence  of  vocal  fremitus  and  rales.  The  conclusive  sign  of  massive 
collapse  of  the  lung  is  displacement  of  the  heart's  apex  beat  toward  the 
affected  side,  and  it  is  the  only  sign  peculiar  to  the  condition  (Pasteur). 

Occasionally  in  the  early  stages  it  may  be  difficult  to  differentiate 
typhoid  fever  and  meningitis  from  the  atypical  forms  of  pneumonia. 
It  is  in  such  cases  that  one  should  always,  whenever  possible,  enlist  the 
aid  of  the  laboratory.  The  confusion  which  sometimes  arises  between 
acute  lobar  pneumonia  and  acute  abdominal  inflammations  have  been 
alluded  to  above. 

FRIEDLANDER'S  BACILLUS  PNEUMONIA 

Etiology. — A  very  fatal  but  fortunately  a  rare  form,  of  pneumonia 
is  that  known  as  Friedlander's  bacillus  pneumonia.  The  exciting  cause 
of  this  type  of  pneumonia  is  the  bacillus  mucosus  capsulatus,  also  known 
as  the  pneumobacillus  and  Friedlander's  bacillus.  Although  this  organ- 
ism was  identified  by  Friedlander  in  1882  it  has  never  attracted  much 
attention  as  one  of  the  causes  of  lobar  pneumonia.  "Thus  far  only 
about  thirty-three  cases  of  pneumonia  have  been  reported  so  fully  that 
they  can  reasonably  be  considered  to  have  been  produced  solely  by  the 
bacillus  mucosus  capsulatus.  Some  of  these  may  be  questioned  as 
unequivocal  cases  of  so-called  'Friedlander  pneumonia.'"1 

The  bacillus  mucosus  capsulatus  is  found  either  as  a  primary  or  a 
secondary  invader  in  about  5  per  cent,  of  all  cases  of  pneumonia.  It  has 
been  noted  also  in  a  considerable  number  of  cases  in  which  the  tubercle 

1Sisson  and  Thompson:  Am.  Jour.  Med.  Sc,  Nov.  15,  1915. 


DISEASES    OF    THE    LUNGS  415 

bacillus  is  the  primary  source  of  infection.  Owing  to  the  fact  that  the 
diagnosis  rests  entirely  on  the  bacteriological  findings  it  is  quite  possible 
that  Friedlander's  bacillus  pneumonia  is  of  more  frequent  occurrence  than 
the  number  of  reported  cases  would  indicate. 

The  organism  may  be  found  in  pure  culture  in  the  sputum  or  in  the 
blood,  the  latter  being  the  most  conclusive  proof. 

This  type  of  pneumonia  occurs  chiefly  in  late  adult  life;  it  is  rarely 
encountered  in  infants  and  young  children. 

Morbid  Anatomy. — A  lung  which  has  become  the  seat  of  pneumonia 
due  to  the  Friedlander  bacillus  presents  certain  characteristics  which 
serve  to  distinguish  it  from  infections  due  to  the  pneumococcus.  The 
cut  surface  lacks  the  granular  appearance  so  characteristic  of  pneu- 
mococcus infections.  In  the  early  stages  the  process  is  more  or  less 
lobular  in  its  distribution  and  hemorrhagic  foci  are  not  uncommon.  This 
gives  the  lung  a  mottled,  marble-like  appearance.  Later  the  lobular 
areas  tend  to  coalesce,  forming  a  more  or  less  homogeneous  appearance. 
The  lung  then  has  a  grayish-slaty  color.  Areas  of  necrosis  and  abscess 
formation  are  not  uncommon  and  are  more  frequently  seen  in  this  form 
of  pneumonia  than  in  pneumococcus  pneumonias.  Practically  the  same 
changes  have  been  demonstrated  in  experimental  animals  by  Sisson  and 
Walker.1  These  observers  found  that  the  lungs  of  cats  infected  with 
the  bacillus  mucosus  capsulatus  showed  in  the  early  stages  a  lobular 
distribution,  which  later  became  homogeneous,  and  the  presence  of 
hemorrhagic  foci.  The  lung  was  at  first  mottled  and  marble-like  in 
appearance,  later  it  became  of  a  grayish  color  and  the  cut  surface  was 
not  granular. 

The  exudate  from  the  lung  is  abundant  and  of  a  slimy,  mucoid  appear- 
ance. A  fibrinous  exudate  is  nearly  always  present  on  the  pleura  and 
this  may  lead  to  a  serofibrinous  or  purulent  effusion.  Occasionally  the 
other  serous  membranes  are  involved. 

Histologically  the  alveoli  are  seen  to  be  filled  with  a  serous  exudate 
containing  red  blood  cells,  pus  cells  and  desquamated  epithelial  cells. 
Fibrin  is  less  abundant  than  in  the -ordinary  type  of  pneumonia.  A 
striking  feature  of  the  disease,  in  most  instances,  is  the  enormous  number 
of  the  infecting  organisms  which  may  be  both  extracellular  and 
intracellular. 

Symptoms. — Aside  from  the  extreme  severity  of  the  constitutional 
symptoms  and  the  brief  duration  of  the  disease  there  is  nothing  clinic- 
ally to  distinguish  this  type  of  pneumonia  from  the  ordinary  form.  It 
more  often  begins  without  a  chill  than  with  one.  Usually  the  onset 
is  with  pain  in  the  side,  cough  and  dyspnea.  Delirium  may  occur  early. 
Herpes  labialis  so  frequently  seen  in  the  pneumococcus  form  rarely  occurs 
in  this  type.  The  evidences  of  a  severe  toxemia  are  marked  and  weak- 
ness, coma,  and  cardiac  failure  may  appear  early  in  the  course  of  the 
disease.  The  temperature  may  be  continuous  or  remittent  and  as  a  rule 
is  not  as  high  as  that  seen  in  the  ordinary  form  and  the  pulse  rate  is  also 
apt  to  be  lower.  Considerable  importance  is  attached  to  the  character 
of  the  sputum.  This  is  abundant,  bloody,  very  slimy,  non-purulent  in 
character  and  contains  great  numbers  of  the  infecting  organism.  A 
leukocytosis  is  commonly  present. 

This  form  of  pneumonia  is  usually  of  brief  duration  and  a  fatal 
1  Jour.  Exp.  Med.,  Dec.  1,  1915. 


416      DISEASES   OF  THE  BRONCHI,   LUNGS,    PLEURA,   AND   DIAPHRAGM 

termination  is  the  rule.  Death  may  occur  in  a  little  over  24  hours" from 
the  onset  of  the  initial  symptoms. 

Physical  Signs. — There  is  nothing  to  distinguish  this  type  from  the 
usual  form  of  pneumonia  so  far  as  physical  examination  is  concerned. 

Diagnosis. — Pneumonia  due  to  the  bacillus  mucosus  capsulatus  may 
be  suspected  in  a  patient  with  signs  of  pulmonary  consolidation,  severe 
toxemia  and  the  presence  of  an  abundant,  sanguineous,  and  slimy 
sputum.  The  definite  proof,  however,  rests  on  the  occurrence  of  large 
numbers  of  the  Friedlander  organism  in  the  sputum  or  in  blood  cultures. 

PSITTACOSIS 

The  term  psittacosis  (from  \}/ltt clkos,  parrot)  is  applied  to  an  infec- 
tious disease  transmitted  to  man  by  parrots, and  characterized  by  a  ty- 
phoid state  and  atypical  pneumonia.  In  parrots  the  disease  is  distin- 
guished by  listlessness,  diarrhea,  and  loss  of  appetite.  The  feathers  stand 
on  end,  the  wings  droop,  and  marked  wasting  and  debility  develop  rapidly. 
The  disease  is  almost  invariably  fatal  in  birds.  Nocard,  in  1893,  isolated 
from  diseased  birds  a  bacillus  which  has  many  of  the  the  cultural  charac- 
teristics of  the  bacillus  typhosus.  This  organism  is  accepted  as  the 
infecting  agent  in  birds  although  it  has  been  found  in  man  in  but  a  single 
instance. 

Etiology. — Although  several  small  house  epidemics  had  been  de- 
scribed prior  to  the  Paris  epidemic  in  1892  and  1893,  it  was  not  until  the 
occurrence  of  the  latter  that  the  disease  attracted  attention. 

The  Paris  epidemic  followed  an  importation  of  parrots  from  South 
America.  There  were  49  cases,  with  16  deaths,  in  1892  and  the  following 
year  7  more  cases  were  observed  with  5  deaths.  Since  that  time  a  num- 
ber of  small  house  epidemics  have  been  noted  in  France,  Italy  and  Ger- 
many. In  this  country  3  probable  cases  of  psittacosis  have  been  reported 
by  Vickery  and  Richardson.1  Up  to  the  present  time  about  100  cases 
have  been  recognized. 

The  disease  is  believed  to  be  transmitted  from  bird  to  man  and  never 
from  man  to  man.  The  infection  may  occur  as  the  result  of  feeding  from 
mouth  to  beak,  a  practice  followed  by  pigeon  raisers  and  which  in  the 
latter  sometimes  causes  infection  with  the  aspergillus.  More  commonly 
the  infection  is  acquired  by  fondling  the  sick  bird  or  by  cleaning  the  con- 
taminated cages. 

Although  the  cases  reported  seem  to  indicate  that  there  is  a  close 
relationship  between  the  disease  occurring  in  parrots  and  that  which 
occurs  in  man  the  proof  is  not  conclusive.  In  the  first  place  the  organism 
isolated  by  Nocard  and  believed  to  be  the  infecting  agent  in  parrots, 
has  been  found  but  once  in  human  beings  nor  have  agglutinating  tests 
been  uniform;  and  in  the  second  place,  relatively  few  individuals  acquire 
the  infection  although  ample  opportunity  is  offered  in  the  case  of  bird 
fanciers  and  those  who  have  parrots  for  pets.  Within  the  past  few  years 
there  has  been  no  reference  to  the  disease  in  the  literature. 

Morbid  Anatomy. — In  parrots  dying  from  the  disease,  the  patholog- 
ical findings  consist  of  a  severe  enteritis  and  cloudy  swelling  of  the  spleen, 
liver  and  kidneys.  Nocard's  organism  is  found  in  the  marrow  of  the 
wing  bones. 

1  Trans.  Assoc.  Am.  Phys.,  1904,  p.  364. 


DISEASES    OF    THE    LUNGS  417 

In  man,  little  is  known  of  the  pathology.  Cases  have  been  recorded 
in  which  a  lobar  or  lobular  type  of  pneumonia  was  found.  Cultures  from 
the  heart's  blood,  the  lungs  and  other  organs  have  shown  the  presence 
of  the  pneumococcus,  streptococcus  and  other  organisms.  Failure  to 
find  Nocard's  organism  is  explained  on  the  ground  that  this  organism 
has  been  killed  off  by  secondary  invaders. 

Symptoms. — Dieulafoy  places  the  incubation  period  at  from  seven 
to  twelve  days,  while  other  observers  state  that  it  may  last  for  as  long  as 
twenty-five  days. 

The  disease  may  be  ushered  in  abruptly  or  it  may  have  an  insidious 
onset.  When  the  onset  is  sudden  the  clinical  picture  is  not  unlike  that 
of  pneumonia.  There  is  a  chill,  marked  prostration,  and  fever  which 
rises  rapidly  to  102°  or  104°F.  and  is  continuous  in  type  with  slight  daily 
remissions.  Cough  appears  early  and  is  usually  attended  with  mucoid, 
rusty  or  bloody  sputum.  In  some  cases  there  is  no  sputum.  Herpes  are 
absent. 

In  other  cases  the  onset  is  insidious  and  bears  a  striking  resemblance 
to  typhoid  fever.  The  patient  complains  of  headache,  malaise,  weakness, 
anorexia  and  diarrhea  or  constipation,  usually  the  latter.  The  breath  is 
foul  and  the  tongue  heavily  coated.  A  petechial  eruption  is  sometimes 
present.  The  spleen  has  been  noted  as  being  enlarged  in  some  cases. 
Delirium,  apathy  or  stupor  is  often  present.  Respiratory  symptoms 
are  also  present  in  the  typhoid  type  of  the  disease. 

A  severe  stomatitis  or  peribuccal  edema  may  be  an  early  manifesta- 
tion in  those  who  have  practised  mouth  to  mouth  feeding. 

The  disease  remains  stationary  for  from  eight  to  ten  days  when  the 
temperature  falls,  usually  by  lysis.  Convalescence  is,  as  a  rule,  pro- 
tracted.    The  total  mortality  for  reported  cases  is  about  30  per  cent. 

Physical  Signs. — Examination  of  the  chest  may  show  the  presence 
of  fine  moist  rales  throughout  both  lungs  or  physical  signs  indicative  of 
either  a  broncho-pneumonia  or  lobar  pneumonia.  Often  the  physical 
findings  are  inconclusive. 

Diagnosis. — This  rests  entirely  on -a  knowledge  of  the  exciting  cause. 
If  it  is  known  that  the  patient  has  been  in  contact  with  a  diseased  parrot, 
psittacosis  should  at  once  suggest  itself.  Especially  should  one's  sus- 
picions be  aroused  if  several  members  of  a  household  are  simultaneously 
affected.  In  the  absence  of  such  knowledge  the  case  is  certain  to  be 
regarded  as  one  of  atypical  pneumonia. 

BRONCHO-PNEUMONIA 

This  form  of  pneumonia  is  also  known  as  catarrhal  pneumonia,  lobular 
pneumonia  and  capillary  bronchitis.  The  latter  term  should  never  be 
used.  While  a  lesion  limited  to  the  finer  bronchioles  is  possible  theoretic- 
ally, practically  it  never  exists  alone,  as  an  inflammatory  process  involv- 
ing the  smaller  bronchi  inevitably  extends  to  the  anatomically  related 
or  contiguous  vesicles  as  well.  The  term  broncho-pneumonia  is  much 
the  most  preferable  designation  and  by  common  consent  is  the  one  now  in 
general  use.  As  the  name  implies  the  process  involves  both  the  bronchi 
and  the  pulmonary  vesicles. 

Etiology. — The  disease  occurs  as  a  primary  and  secondary  manifesta- 
tion and  is  encountered  most  frequently  at  the  two  extremes  of  life.     The 

27 


418      DISEASES   OF  THE  BRONCHI,    LUNGS,    PLEURA,   AND   DIAPHRAGM 

two  sexes  are  about  equally  affected.  The  primary  form  is  almost  invari- 
ably seen  in  children  under  two  years  of  age.  Beyond  this  age  period 
the  disease  is  usually  a  secondary  manifestation.  Statistics  show  that 
in  about  one-third  of  all  cases  the  disease  is  primary. 

As  a  secondary  manifestation  broncho-pneumonia  occurs  under  a 
variety  of  conditions. 

(a)  As  a  complication  of  or  sequel  to  one  of  the  acute  infectious  dis- 
eases broncho-pneumonia  is  encountered  with  great  frequency.  While 
any  of  the  acute  infections  may  give  rise  to  broncho-pneumonia  the  infec- 
tions most  to  be  feared  are  diphtheria,  measles  and  whooping  cough. 
There  is  a  very  widespread  belief  among  the  laity  that  measles  and 
whooping  cough,  especially  the  latter,  are  relatively  harmless  affections. 
For  this  reason  children  are  often  purposely  exposed  to  these  diseases  in 
order  that  what  is  believed  to  be  a  necessary  episode  in  their  lives  may 
be  over  and  done  with.  Although  both  these  diseases  are  relatively 
harmless  in  themselves  it  cannot  be  too  strongly  insisted  upon  that  they 
are  extremely  dangerous  because  of  their  complications  and  sequels.  A 
very  considerable  proportion  of  deaths  from  broncho-pneumonia  occur 
in  children  in  whom  the  primary  infection  was  either  measles  or  whooping 
cough. 

(b)  In  both  children  and  adults  broncho-pneumonia  may  succeed  an 
attack  of  acute  bronchitis,  the  inflammatory  process  extending  along 
the  bronchial  tubes  and  eventually  implicating  the  air  vesicles.  A 
secondary  broncho-pneumonia  may  arise  also  in  cases  of  bronchiectasis, 
chronic  interstitial  pneumonia,  pulmonary  abscess  or  as  a  result  of  an 
empyema  rupturing  into  the  lung.  In  like  manner  broncho-pneumonia 
may  occur  in  cases  of  chronic  tuberculosis  with  cavity  formation,  the 
infecting  material  from  the  cavity  giving  rise  to  an  ordinary  broncho- 
pneumonia, a  tuberculous  broncho-pneumonia  or  both. 

(c)  A  focus  of  infection  anywhere  in  the  body  may  by  metastasis 
give  rise  to  a  septic  broncho-pneumonia.  Among  such  conditions  may  be 
mentioned  acute  otitis  media,  suppurative  appendicitis,  salpingitis,  in- 
fections of  the  urinary  tract,  etc. 

(d)  Broncho-pneumonia  is  to  be  classed  among  the  most  frequent 
of  the  terminal  infections.  In  the  aged  and  debilitated  and  in  those 
suffering  from  some  chronic  affection  such  as  heart  disease,  nephritis, 
malignant  disease,  diabetes,  etc.,  it  is  one  of  the  most  frequent  causes 
of  death. 

(e)  Still  another  form  of  the  disease  is  the  so-called  inhalation  or 
deglutition  pneumonia.  In  health  the  sensitiveness  of  the  larynx  pre- 
vents the  passage  of  food  and  drink  into  the  trachea  and  bronchi.  If, 
however,  the  larynx  becomes  insensitive  as  the  result  of  the  narcotic 
effect  of  alcohol,  ether  or  chloroform  or  as  the  result  of  stupor  or  un- 
consciousness, such  as  occurs  in  uremia,  apoplexy,  etc.,  food  or  drink  or 
septic  material  may  be  aspirated  into  the  lungs  and  set  up  a  very  severe 
form  of  broncho-pneumonia. 

Aspiration  pneumonia  may  also  follow  the  inhalation  of  material 
from  a  bronchiectatic  cavity,  a  tuberculous  cavity  or  it  may  occur  as  a 
sequel  to  a  large  hemoptysis.  This  form  of  the  disease  not  infrequently 
follows  operations  about  the  nose,  mouth  or  larynx. 

Children  who  are  debilitated  as  the  result  of  syphilis,  rickets  or  diar- 
rhea are  extremely  subject  to  broncho-pneumonia,  and  children  living 


DISEASES    OF    THE    LUNGS 


419 


amidst  insanitary  surroundings  and  inmates  of  orphan  asylums  or  found- 
ling homes  are  especially  prone  to  develop  the  disease. 

Inasmuch  as  broncho-pneumonia  frequently  develops  as  a  sequel  to 
acute  bronchitis  the  disease  is  usually  more  prevalent  during  the  winter 
and  early  spring  months.  At  this  time  respiratory  infections  are  far  more 
common  than  at  other  seasons  of  the  year  and  in  this  respect  broncho- 
pneumonia is  no  exception. 

Morbid  Anatomy. — The  affection  is  nearly  always  bilateral,  although 
the  lesions  may  be  much  more  extensive  on  one  side  than  the  other.  Holt 
found  the  disease  bilateral  in  82  per  cent,  of  cases  coming  to  autopsy. 


Fig.  276. — Lobular  pneumonia  in  adult  lung,  showing  patchy  areas  of  consolidation. 
(MacCallum's  Pathology.) 

The  disease  has  a  decided  preference  for  the  posterior  aspect  of  the  lower 
lobes.     The  middle  lobe  of  the  right  lung  is  the  least  affected  portion. 

A  lung  the  seat  of  a  broncho-pneumonic  process  is  heavier  than  normal, 
deeply  congested  and  while  crepitant  throughout,  reveals  to  the  touch 
scattered  nodules  of  consolidation  (Fig.  276).  Pleurisy  is  less  common  in 
the  broncho-pneumonic  form  than  in  the  lobar  type  of  the  disease. 


420         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

When  the  lesion  is  just  beneath  the  pleura  the  latter  may  be  slightly 
clouded  or  there  may  be  a  deposit  of  fibrin  or  purulent  material.  Oc- 
casionally a  moderate-sized  effusion  may  occur. 

A  very  common  finding,  especially  in  young  children,  are  areas  of 
atelectasis.  The  most  frequent  sites  of  the  collapsed  vesicles  are  the 
posterior  inferior  margins  of  the  lower  lobes,  the  free  margins  of  the  lung 
anteriorly  and  at  times  the  inner  margin  of  the  lungs  adjacent  to  the 
spine.  The  atelectatic  area  is  sharply  defined,  shrunken,  depressed  below 
the  surface  and  of  a  bluish  or  dark  violet  tint.  On  section  it  is  smooth 
and  glistening  in  appearance  and  on  pressure  a  small  amount  of  bloody 
serum  exudes.  The  tissue  not  only  feels  airless  but  also  sinks  when  placed 
in  water.  About  the  collapsed  areas  the  pulmonary  tissue  may  be 
edematous  or  show  compensatory  emphysema.  On  section  the  broncho- 
pneumonic  process  shows  an  intense  congestion  of  the  bronchial  mucous 
membrane  and  small  groups  of  vesicles.  The  smaller  bronchi  and 
bronchioles  and  the  affected  air  cells  are  completely  filled  with  an  inflam- 
matory exudate  which  contains  little  or  no  fibrin.  The  exudate  consists 
mainly  of  serum,  a  few  red  cells,  numerous  leukocytes  and  large  mono- 
nuclear or  catarrhal  cells. 

The  patches  of  consolidation  vary  greatly  in  size.  They  may  consist 
of  small  foci  the  size  of  a  pinhead  or  be  as  large  as  a  hazelnut.  A  number 
of  distinct  foci  may  merge  into  each  other  producing  a  large  area  resem- 
bling croupous  pneumonia.  Occasionally  in  young  children  a  fulminant 
type  of  the  disease  occurs  in  which  death  occurs  before  consolidation 
becomes  evident. 

On  section  of  the  lung  the  broncho-pneumonic  area  is  seen  to  project 
slightly  above  the  cut  surface  and  is  more  or  less  sharply  circumscribed. 
At  first  the  lesion  is  firm  and  reddish  in  color  but  in  its  later  stages  it  is 
reddish  gray,  gray,  or  yellowish  in  color  and  very  friable.  On  pressure 
a  turbid  blood-stained  fluid  can  be  expressed  in  which  may  be  seen 
purulent  material. 

In  the  aspiration  forms  of  the  disease  numerous  small  abscesses  may 
develop  at  the  site  of  the  lesions.  When  the  disease  runs  a  protracted 
course  the  tubercle  bacillus  is  to  be  suspected.  In  children  a  widespread 
tuberculous  broncho-pneumonia  is  not  an  uncommon  finding.  In  fatal 
cases  abscess  formation  is  not  infrequent  but  gangrene  is  rare.  When 
recovery  takes  place  the  consolidated  areas  undergo  complete  resolution 
in  the  great  majority  of  cases.  In  some  instances  a  rather  diffuse  bilateral 
fibrosis  and  bronchiectasis  follow  an  attack  of  broncho-pneumonia. 

Bacteriology. — Mixed  infections  are  almost  the  rule  in  broncho- 
pneumonia, the  streptococcus  being  the  most  constant  organism.  Among 
the  organisms  which  have  been  found  alone  or  in  association  with  others 
may  be  mentioned  the  pneumococcus,  streptococcus,  staphylococcus 
aureus  and  albus,  Friedlander's  bacillus,  the  influenza  bacillus,  the 
diphtheria  bacillus,  etc.  Neither  the  symptoms  nor  the  pulmonary  in- 
volvement show  any  marked  differences  as  the  result  of  infection  by 
different  organisms. 

Symptoms. — The  recognition  of  broncho-pneumonia  is  not  easy 
because  of  the  varied  clinical  picture.  Then,  too,  in  infants  the  disease 
is,  at  times,  so  violent  that  death  may  ensue  in  from  12  to  24  hours,  and 
before  the  true  nature  of  the  trouble  is  appreciated.  In  marked  contrast 
is  the  insidious  onset  and  the  paucity  of  both  symptoms  and  physical 


DISEASES    OF    THE    LUNGS  421 

signs  which  so  frequently  characterize  the  disease  in  the  debilitated  and 
the  aged. 

In  the  primary  form  of  the  disease  which  occurs  almost  exclusively 
in  children  under  two  years  of  age,  the  onset  is  usually  sudden  with  a 
chill  or  convulsion.  The  temperature  rises  rapidly  and  is  usually  con- 
tinuous in  type.  In  many  cases  cerebral  symptoms  play  a  prominent 
part  and  may  dominate  the  picture  leading  to  a  diagnosis  of  meningitis. 
The  child  is  peevish,  very  restless,  easily  excited,  is  sleepless  and  often 
very  delirious.  The  disease  often  terminates  by  crisis.  The  mortality 
from  primary  broncho-pneumonia  is  slight.  Owing  to  the  presence  of 
physical  signs  indicating  consolidation  of  the  lung  the  condition  is  often 
mistaken  for  lobar  pneumonia. 

In  the  secondary  form,  both  the  onset  and  course  of  the  disease  are 
essentially  different.  Instead  of  a  sudden  onset  in  a  child  previously 
well  there  has  been  present  an  acute  bronchitis  either  alone  or  as  a  com- 
plication of  one  of  the  acute  infections,  particularly  measles  or  whooping 
cough.  The  transition  from  the  minor  to  the  serious  affection  is  gradual 
and  the  first  thing  to  arouse  suspicion  as  to  the  presence  of  broncho-pneu- 
monia may  be  the  increase  in  the  respiratory  rate  and  an  accession  of 
fever.  In  a  child  convalescing  from  measles  or  whooping  cough  the  oc- 
currence of  these  symptoms  and  the  presence  of  rales  in  the  lungs,  even 
without  evidence  of  consolidation,  are  sufficient  to  warrant  a  diagnosis 
of  broncho-pneumonia. 

The  fever  is  usually  moderately  high  and  may  be  either  remittent 
or  intermittent  in  type.  Usually  the  difference  between  the  morning  and 
evening  temperatures  amounts  to  3°F.  or  more  (Fig.  277).  Occasionally 
there  may  be  hyperpyrexia  while  in  weak  and  debilitated  children  the 
temperature  may  be  but  slightly  elevated  or  even  subnormal.  In 
secondary  broncho-pneumonia  the  temperature  always  falls  by  lysis, 
the  febrile  period  lasting  from  one  to  three  weeks. 

The  pulse  is  usually  very  rapid  but  the  increase  in  frequency  is 
relatively  less  than  that  of  the  respiration.  If  the  embarrassment  of 
the  right  heart  is  marked  the  pulse  r-ate  runs  up  to  150  or  higher  and  is 
apt  to  be  irregular. 

The  respiratory  rate  is  markedly  increased  and  in  severe  cases  the 
intense  dyspnea  may  be  the  most  striking  feature  of  the  disease.  A 
respiratory  rate  of  50  or  more  is  not  uncommon.  The  difficulty  in 
breathing  is  usually  in  proportion  to  the  extent  of  the  pulmonary  in- 
volvement. In  fatal  cases  marked  dyspnea  is  frequently  associated 
with  atelectasis.  In  addition  to  the  respiratory  distress  deficient  aera- 
tion of  the  blood  is  shown  by  the  cyanosis  of  the  face  and  finger  tips  and 
the  anxious  expression.  In  the  severe  fatal  cases  the  child  rapidly  passes 
into  a  condition  of  asphyxia.  " 

Pain  is  rarely  a  marked  feature  in  this  form  of  pneumonia  and  in 
many  cases  is  entirely  absent.  It  usually  occurs  in  the  form  of  a  dull 
aching  sensation  over  the  site  of  the  pulmonary  lesion. 

Cough  is  usually  a  prominent  feature  and  is  often  very  distressing. 
A  vigorous  cough  indicates  absence  of  toxemia  while  a  feeble  cough  or 
the  cessation  of  cough  is  usually  associated  with  severe  cases.  In  children 
the  sputum  is  usually  swallowed.  In  adults  it  may  consist  of  a  thin 
mucus  or  it  may  be  mucopurulent  in  character.  ( )ccasionally  the  sputum 
is  blood  streaked. 


422         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA.    AND    DIAPHRAGM 


Tjie  gkin. — In  severe  eases  with  extensive  pulmonary  lesions  there 
is  usually  some  evidence  of  cyanosis  clue  to  the  embarrassed  right  heart. 
In  such  cases  the  tips  of  the  ears,  the  lips  and  the  finger  tips  are  of  a 
dusky  hue.     When  cyanosis  is  present,  the  skin  is  apt  to  be  cool  and 


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clammy  Ordinarily  the  skin  feels  hot  and  slightly  moist,  Sweating 
often  occurs  during' the  height  of  the  disease.  Herpes  labiahs  so  com- 
monly met  with  in  the  lobar  form  of  pneumonia  are  rarely  seen  in 
broncho-pneumonia . 


DISEASES    OF   THE    LUNGS  423 

Gastro-intestinal  symptoms  are  common.  A  child  ill  with  broncho- 
pneumonia usually  refuses  food.  Thirst  is  marked.  Vomiting  is  a 
common  symptom  and  in  addition  there  is  often  diarrhea,  the  stools 
being  green  in  color  and  containing  mucus  and  undigested  food. 

Nervous  symptoms  are  often  very  marked  especially  in  severe 
cases.  The  child  is  restless,  irritable,  sleeps  poorly  and  at  times  is 
delirious. 

The  urine  presents  the  usual  characteristics  seen  in  fever  patients. 
It  is  scanty,  high-colored,  shows  a  trace  of  albumen  and  there  also  may 
be  tube  casts. 

In  adults  broncho-pneumonia  is  less  common  than  the  lobar  form. 
It  is  always  secondary  and  presents  the  same  clinical  picture  as  that  just 
given  for  children. 

The  duration  of  an  attack  of  broncho-pneumonia  is  variable.  We 
have  alluded  already  to  the  fulminant  type  in  which  death  may  occur 
within  48  hours.  In  the  average  case  the  disease  runs  its  course  in  from 
two  to  three  weeks.  It  may  terminate,  however,  in  a  week  or  it  may  be 
prolonged  beyond  three  weeks.  In  the  protracted  form  described  by 
Holt  the  disease  may  last  for  four  or  five  weeks  or  even  longer.  In  this 
type  of  the  disease  the  fever  persists  but  is  subject  to  exacerbations  and 
remissions.  The  child  wastes,  becomes  anemic,  profoundly  prostrated 
and  finally  dies  from  slow  asthenia.  The  clinical  picture  is  strikingly 
similar  to  tuberculous  broncho-pneumonia  and  the  distinction  between 
the  two  is  not  easy. 

Broncho-pneumonia  as  it  occurs  in  the  aged  and  debilitated  very  often 
begins  insidiously  and  neither  the  symptoms  nor  the  physical  signs  are 
distinctive.  As  a  result  the  disease  often  escapes  detection  during  life 
and  is  first  discovered  at  the  autopsy. 

During  the  winter  and  spring  months  when  pulmonary  diseases  are 
most  common  even  trivial  respiratory  symptoms  are  to  be  viewed  with 
suspicion  when  occurring  in  those  of  advanced  years  and  in  those  debili- 
tated from  some  chronic  disease.  The  most  significant  symptoms  are 
fever,  cough  and  dyspnea,  especially  in  one  who  is  already  suffering  from 
bronchitis.  Physical  examination  may  show  the  presence  of  a  diffuse 
bronchitis  with  or  without  patches  of  consolidation.  In  some  instances 
there  is  an  absence  of  symptoms ;  in  others  it  may  be  impossible  to  detect 
any  evidence  of  a  pulmonary  lesion  and  in  still  others,  both  symptoms  and 
signs  may  be  so  indefinite  as  to  entirely  escape  notice.  A  knowledge  of 
the  frequency  with  which  broncho-pneumonia  occurs  as  a  terminal  in- 
fection in  the  aged  and  debilitated  should  make  one  alert  in  the  presence 
of  even  the  most  trifling  respiratory  symptoms. 

An  extremely  fatal  form  of  broncho-pneumonia  is  that  in  which 
the  exciting  organism  is  the  Bacillus  pestis.  During  a  plague  epidemic 
the  pneumonic  type  of  the  disease  is  encountered  in  a  small  percentage  of 
cases.  The  infection  may  be  primary  due  to  the  inhalation  of  plague 
bacilli  which  have  sprayed  into  the  air  by  coughing  or  it  may  occur 
secondarily  to  a  focus  elsewhere  in  the  body. 

This  form  of  broncho-pneumonia  is  characterized  by  an  abrupt  onset 
with  a  chill,  fever  which  may  be  continuous  or  remittent,  dyspnea,  cyano- 
sis, cough  and  the  expectoration  of  mucopurulent,  blood-streaked,  or 
hemorrhagic  sputum. 

The  physical  signs  are  those  indicative  of   patches  of  consolidation 


424  DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AXD    DIAPHRAGM 

in  the  lower  lobes  posteriorly.  Physical  examination  also  shows  marked 
enlargement  of  the  spleen. 

Physical  Signs. — The  physical  signs  of  broncho-pneumonia  do  not 
lend  themselves  readily  to  description.  If.  however,  one  keeps  in  mind 
the  pathology  of  the  disease,  the  irregularity  of  the  physical  findings  is 
more  easily  understood.  In  children  and  to  some  extent  in  adults,  this 
is  facilitated  by  following  the  classification  of  Holt  who  describes: 

(1)  The  stage  of  congestion  without  consolidation.  (2)  The  stage  of 
partial  consolidation.  (3)  The  stage  with  areas  more  or  less  completely 
consolidated.     (4)  The  prolonged  form. 

First.  The  Stage  of  Congestion.- — Inspection. — The  breathing  is 
rapid  and  shallow,  the  lower  intercostal  spaces,  the  submammary  region 
and  the  epigastrium  receding  with  inspiration.  These  signs  are  more 
marked  in  infants  than  in  those  of  mature  years. 

Palpation. — Palpation  is  negative  except  for  the  occasional  occurrence 
of  rhonchial  fremitus. 

Percussion. — In  the  early  stages  of  the  disease  the  percussion  note 
may  be,  and  usually  is,  normal,  a  fact  that  Holt  has  especially  emphasized. 
At  the  most,  there  may  be  a  slight  area  at  one  base  near  the  spine,  in  which 
the  percussion  note  deviates  slightly  from  the  normal. 

Auscultation. — -As  a  primary  infection,  the  signs  are  those  of  a  bron- 
chitis affecting  the  smaller  tubes,  while  if  the  disease  develops  from  a 
preexisting  bronchitis  of  the  larger  tubes,  the  rales  are  of  a  mixed  char- 
acter. In  the  beginning  the  breathing  may  be  normal  everywhere,  but 
sooner  or  later  localizing  signs  in  the  form  of  very  fine,  moist  rales 
(subcrepitant)  appear,  usually  at  one  or  other  of  the  bases.  Over  this 
area  the  breath  sounds  may  then  become  feebler  and  higher  in  pitch. 
The  voice  sounds  may  also  become  more  intense  and  higher-pitched 
(see  Figs.  278  and  279). 

Second.  Stage  of  Partial  Consolidation. — Inspection. — Xo 
change. 

Palpation. — Over  the  area  of  partial  consolidation  the  tactile  fremitus 
may  be  increased. 

Percussion. — While  the  auscultatory  signs  of  consolidation  are  apt 
to  be  well  marked  in  this  stage,  the  percussion  changes  are  much  less  so, 
and  may  be  negative.  This  is  ascribed  to  the  superficial  nature  of  the 
lesions,  and  by  the  fact  that  the  small  consolidated  areas  are  separated 
by  normal  vesicular  tissue.  If  impairment  over  a  limited  area  has 
been  noted  previously,  however,  it  is  apt  to  be  more  pronounced,  and  the 
area  of  slight  impairment  considerably  extended.  Slight  changes  in  the 
percussion  note  may  be  detected  at  this  time  over  the  opposite  lung,  or 
over  another  portion  of  the  same  lung. 

Auscultation. — In  addition  to  the  auscultatory  findings  noted  in  the 
first  stages,  there  are  added  those  of  more  or  less  complete  consolidation, 
namely,  enfeebled  breathing,  bronchial  in  character,  bronchophony  and 
whispering  pectoriloquy. 

Third.  With  Areas  of  Consolidation  More  or  Less  Complete.- — 
Palpation. — Over  the  area  of  consolidation  the  tactile  fremitus  is  usually 
increased. 

Percussion. — The  note  is  dull  but  not  markedly  so  owing  to  the  fact 
that  the  lesion  is  superficial  and  does  not  extend  very  deeply  into  the  lung. 

Auscultation. — Over  the  central  portion  of  the  consolidated  area  the 


DISEASES    OF    THE    LUNGS 


425 


breathing  is  bronchial.  As  the  periphery  of  this  area  is  approached  the 
breath  sounds  become  less  bronchial  and  in  addition  rales  are  heard. 
The  vocal  fremitus  is  increased  (see  Figs.  280  and  281). 


Fig.  278. — First  stage.  Coarse  rales  over 
both  lungs;  localized  fine  (subcrepitant) 
rales  at  the  left  base.  Xo  change  in  breath- 
ing sounds.     (Holt.) 


Fig.  279. — Second  stage.  Coarse  and  fine 
rales  over  both  lungs  behind;  at  left  base  an 
area  of  partial  consolidation,  with  broncho- 
vesicular  breathing,  exaggerated  voice,  and 
very  sharp  rales.     (Holt.) 


Fig.  280. — Third  stage.  A  larger  area  of 
partial  consolidation,  and  in  the  center  a 
small  area  of  complete  consolidation,  with 
bronchial  breathing  and  voice,  and  slight 
dulness.  Signs  over  the  right  lung  similar 
to  what  were  previously  present  over  the 
left.     (Holt.) 


Fig.  281. — Fourth  stage.  Extensive  dis- 
ease of  both  sides;  large  area  of  complete 
consolidation  on  the  left,  with  dulness, 
bronchial  breathing  and  voice,  and  no  rales; 
surrounding  this  broncho-vesicular  breath- 
ing, with  many  rales.  Signs  in  the  right 
lung  similar  to  those  previously  present  <••,  er 
the  left.  (Holt.) 
Note. — The  disease  may  stop  at  any  one  of  these  stages  and  resolution  take  place. 

The  signs  of  consolidation  may  extend  as  far  forward  as  the  axillary 
line  but  they  usually  stop  there. 

Fourth.  The  Protracted  Form. — In  this  type  the  disease  behaves 
for  three  or  four  weeks  as  an  ordinary  case  of  broncho-pneumonia.     Then 


426  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

instead  of  the  process  subsiding  the  symptoms  persist  and  the  con- 
solidated areas  are  noted  to  gradually  extend  until  the  greater  portion 
of  both  lungs  posteriorly  are  involved.  Over  this  area  there  is  marked 
dulness,  exaggerated  bronchial  breathing  and  bronchophony. 

In  the  adult  the  physical  signs  are  essentially  the  same  as  those  found 
in  the  child. 

In  all  forms  of  broncho-pneumonia  and  especially  as  it  occurs  in  those 
of  advanced  years  and  those  debilitated  by  some  chronic  disease,  there 
may  never  be  airy  signs  pointing  to  consolidation  of  the  lung  tissue  as 
the  lesions  may  be  small  and  widely  scattered.  Holt  emphasizes  the 
following  points:  (1)  That  where  there  is  consolidation  it  is  usually 
incomplete,  because  there  are  small  areas  of  healthy  lung  tissue  between 
the  hepatized  portions;  (2)  that  the  signs  of  consolidation  usually  shade 
off  gradually;  and  (3)  that  both  sides  are  almost  invariably  involved, 
although  one  side  usually  to  a  greater  degree  than  the  other. 

Complications  and  Sequels. — Complications  are  not  as  frequently 
encountered  in  broncho-pneumonia  as  in  the  lobar  form.  Occasionally 
pericarditis  and  endocarditis  occur  but  not  often.  Pleurisy  with  or 
without  an  effusion  is  not  common.  In  children  especially  in  those  under 
bad  hygienic  conditions,  various  forms  of  stomatitis  and  gastro-enteritis 
are  frequently  seen.  Purulent  meningitis  is  relatively  uncommon. 
Small  multiple  abscesses  ma}^  occur  especially  in  the  aspiration  and 
metastatic  types  of  the  disease.  As  a  rule  in  the  cases  which  recover 
resolution  is  complete  but  in  some  instances  a  diffuse  fibrosis  of  the 
lungs  takes  place.  This  may  be  associated  with  dilatation  of  the 
bronchi. 

Diagnosis. — Primary  broncho-pneumonia  in  which  the  onset  is  sud- 
den may  be  confused  with  the  lobar  form.  It  is  to  be  borne  in  mind 
that  broncho-pneumonia  occurs  almost  exclusively  in  children  under 
two  years  of  age  and  that  lobar  pneumonia  is  unusual  at  this  age. 
While  the  area  of  consolidation  may  simulate  that  found  in  lobar  pneu- 
monia a  careful  examination  will  usually  show  a  smaller  focus  on  the 
opposite  side.  In  adults  the  distinction  between  secondary  broncho- 
pneumonia and  frank  lobar  pneumonia  is  usually  easy.  The  onset, 
symptoms  and  plxysical  signs  are  radically  different.  In  atypical  cases 
of  lobar  pneumonia,  especially  in  the  aged,  mistakes  are  frequently 
made.  In  young  infants  confusion  may  arise  as  to  whether  we  have  to  do 
with  broncho-pneumonia  or  congenital  atelectasis.  If  the  latter  is  present 
the  temperature  is  often  subnormal  and  the  cyanosis  marked.  Physical 
signs  are  scanty  or  absent.  In  a  child  previously  healthy  the  occurrence 
of  cough,  fever,  dyspnea  and  cyanosis  points  to  broncho-pneumonia  and 
in  such  cases  the  physical  signs  are  usualty  distinctive. 

The  differentiation  between  tuberculous  and  non-tuberculous  broncho- 
pneumonia  is  not  easj^.  Confusion  is  most  apt  to  occur  in  those  cases 
in  which  the  disease  is  prolonged  beyond  three  or  four  weeks.  As  a  rule 
the  symptoms  are  more  pronounced  in  the  tuberculous  form  and  the 
wasting  and  prostration  are  greater.  While  tuberculous  broncho-pneu- 
monia may  involve  any  portion  of  the  lungs  the  localization  of  signs  at 
the  apex  or  in  the  axilla  are  suggestive  of  this  type  as  the  non-tuberculous 
form  shows  a  marked  preference  for  the  posterior  and  inferior  portions 
of  the  lungs.  If  sputum  can  be  obtained  either  from  vomited  material 
or  by  swabbing  the  back  of  the  throat,  the  detection  of  tubercle  bacilli 


DISEASES    OF   THE    LUNGS  427 

at  once  determines  the  diagnosis.     In  children  under  two  years  of  age 
a  positive  tuberculin  reaction  is  extremely  suggestive. 

In  cases  with  marked  nervous  symptoms  the  distinction  between 
broncho-pneumonia  and  meningitis  is  often  difficult.  In  such  cases  a 
lumbar  puncture  should  always  be  performed. 

Pulmonary  Fibrosis 

This  condition  is  variously  designated  as  chronic  pneumonia,  inter- 
stitial pneumonia  and  cirrhosis  of  the  lung.  In  the  older  literature  on 
the  subject  the  term  fibroid  phthisis  is  frequently  used.  The  latter 
term  is  misleading,  however,  and  should  never  be  applied  to  this  affec- 
tion but  should  be  restricted  to  those  cases  in  which  the  tubercle  bacillus 
is  the  exciting  cause  of  the  fibrosis. 

Fibrosis  of  the  lungs  is  of  interest  because  of  the  similar  effects  and 
symptoms  produced  by  a  lesion  which  is  the  common  result  of  many 
different  processes.  Properly  speaking,  it  is  not  a  disease;  it  is  simply 
the  result  of  some  previous  pulmonary  affection.  While  the  etiological 
and  pathological  features  of  pulmonary  fibrosis  are  extremely  varied  the 
clinical  picture  is  fairly  characteristic  and  it  is  for  this  reason  that  cases 
of  this  nature  are  grouped  together. 

Etiology. — The  etiology  of  fibrosis  of  the  lungs  embraces  practically 
every  disease  to  which  the  lung  is  subject,  whether  acute  or  chronic. 
The  chronicity  of  the  primary  affection,  however,  undoubtedly  has  a 
great  deal  to  do  with  the  process.  Thus,  while  it  is  recognized  that  the 
acute  pulmonary  affections,  as  broncho-pneumonia  or  croupous  pneu- 
monia, may  terminate  in  an  interstitial  pneumonia,  it  is  the  chronic 
affections  that  furnish  the  greatest  number  of  examples  of  the  condition. 

Of  the  chronic  pulmonary  infections  tuberculosis  is  generally  regarded 
as  being  the  most  potent  factor  in  the  production  of  fibrosis.  In  the 
majority  of  cases  the  tuberculous  origin. of  the  fibrosis  can  be  determined 
by  the  presence  of  tubercle  bacilli  in  the  sputum.  Occasionally,  however, 
as  in  a  case  observed  at  the  Phipps  Institute,  tubercle  bacilli  are  not  de- 
tected during  life  and  the  true  nature  of  the  fibrosis  is  revealed  only  by  a 
histological  examination  of  the  lungs. 

One  of  the  most  frequent  of  post-mortem  findings  is  a  small  indurated 
area  in  one  or  the  other  of  the  pulmonary  apices.  Such  areas  are  believed 
to  be  evidences  of  a  healed  tuberculous  focus  although  there  is  no  definite 
proof  that  such  is  always  the  case  as  most  of  them  show  neither  tubercle 
bacilli  nor  any  histological  evidence  of  tuberculosis. 

The  next  most  potent  factor  in  the  production  of  pulmonary  fibrosis 
is  dust.  Under  these  circumstances  the  fibrosis  is  bilateral  and  diffuse. 
This  aspect  of  the  subject  has  been  dealt  with  fully  in  the  chapter  on 
Pneumoconiosis. 

The  acute  inflammatory  affections  of  the  lungs  furnish  relatively  few 
examples  of  the  condition. 

Among  the  rarer  causes  of  pulmonary  fibrosis  may  be  mentioned 
syphilis,  abscess,  infarct  and  the  mycotic  infections.  Chronic  passive 
congestion  sometimes  leads  to  interstitial  changes,  known  as  "  brown 
induration."  This  is  an  unusual  cause.  In  such  instances  the  lung 
not  only  shows  an  overgrowth  of  fibrous  tissue  but,  in  addition,  it  is 
of  a  brownish  red  color  due  to  the  dcposil  of  hemoglobin. 


428  DISEASES    OF    THE    BRONCHI,    LUXGS,    PLEURA,    AXD    DIAPHRAGM 

In  addition  to  the  intrapulmonary  affections,  extrapulmonary  condi- 
tions, as  aneurisms,  mediastinal  growths,  and  pleural  effusions  may 
produce  an  overgrowth  of  fibrous  tissue.  The  importance  of  pleural 
effusions,  especially  when  purulent,  has  been  underestimated.  An  empy- 
ema is  not  an  infrequent  sequel  of  pneumonia  and  very  often  it  is  encysted. 
If  the  effusion  is  not  detected  and  removed  it  acts  as  a  foreign  body  and 
by  reason  of  the  pressure  it  exerts  on  the  pulmonary  tissue,  leads  to  inter- 
stitial changes. 

Morbid  Anatomy. — Fibrosis  of  the  lung  presents  an  extremely  varied 
appearance  pathologically — a  fact  that  has  had  not  a  little  to  do  with 
the  diversity  of  names  under  which  the  condition  has  been  described. 
Any  one  of  the  several  parts  comprising  the  lung  may  be  the  starting 
point  of  the  fibrosis:  the  tissue  about  the  bronchi  and  blood-vessels,  the 
interlobular  septa,  the  alveolar  walls,  or  the  pleura.  When  the  process 
has  been  of  long  standing,  all  of  these  structures  may  become  involved, 
and  any  trace  of  the  original  starting  place  be  obliterated. 

The  varied  conditions  under  which  the  fibrosis  may  arise  and  the 
predominance  of  the  lesion  in  one  or  the  other  of  the  structures  first 
attacked  render  a  satisfactory  classification  impossible.  For  the  sake 
of  convenience  most  writers  recognize  a  local  and  a  massive  type.  Local- 
ized areas  of  fibrosis  are  often  seen.  The  most  common  example  is  that 
so  frequently  encountered  at  the  extreme  apex  of  the  lung. 

The  massive  type  is  of  the  most  interest,  both  pathologically  and 
clinically,  and  the  great  majority  of  cases  seen  and  recognized  as  fibrosis 
belong  to  this  group.  The  massive  type  of  fibrosis  may  be  further  di- 
vided into  a  tuberculous  and  a  non-tuberculous  form.  While  the  ulti- 
mate clinical  picture  is  frequently  identical  in  the  two  forms,  the  early 
stages  differ. 

In  the  tuberculous  form  the  process  starts  at  the  apex,  while  fibrosis 
arising  from  other  cause  most  frequently  has  its  origin  at  the  base  or 
root  of  the  lung.  This  is  of  considerable  importance  in  differentiating 
the  two  forms  when  tubercle  bacilli  are  absent.  It  must  be  borne  in 
mind,  however,  that  non-tuberculous  fibrosis  of  an  upper  lobe  does  occur, 
and  when  associated  with  bronchiectasis  is  often  clinically  indistinguish- 
able from  healed  tuberculosis  with  cavity  formation — a  point  Jacobi  has 
especially  emphasized  (see  Fig.  221).  In  either  case  the  disease  is 
unilateral,  the  affected  side  is  sunken,  the  spine  bowed,  and  the  shoulder 
depressed.  On  opening  the  chest  the  heart  is  seen  to  be  drawn  toward 
the  affected  side  and  the  unaffected  lung  voluminous. 

The  organ  on  removal  is  found  to  be  hard  and  airless  and  strongly 
resists  cutting.  In  the  extreme  grades  the  entire  lung  may  be  reduced  to 
a  mass  of  fibro-cartilaginous  tissue  with  dilated  bronchi.  Between  this 
and  the  lesser  degrees  of  involvement  all  gradations  exist.  The  fibrous 
involvement  is  distinguished  by  the  areas  of  grayish  tissue,  which  may 
be  most  prominent  at  the  root  of  the  lung,  with  radiating  bands  extend- 
ing toward  the  periphery  (Fig.  282),  along  the  interlobular  septa  or  about 
the  bronchi  and  blood-vessels.  Fig.  283  represents  a  type  of  fibrosis 
described  by  Kidd  and  W.  McCollum,  and  termed  by  them  reticular. 
In  this  specimen  the  lung  is  seen  to  be  intersected  by  fibrous  strands 
which  follow  the  interlobular  septa.  This  specimen  also  shows  the 
embedding  of  the  bronchi  and  blood-vessels  in  the  masses  of  fibroid 
tissue. 


DISEASES    OF    THE    LUNGS 


429 


An  almost  constant  feature  of  these  unilateral  cases  is  the  associated 
pleural  thickening.  The  pleural  cavity  becomes  obliterated  and  the 
lung  is  bound  down  by  dense  adhesions,  so  that  it  is  removed  from  the 
chest  cavity  only  with  the  greatest  difficulty.  As  a  rule,  fibroid  changes 
in  the  pleura  form  a  part  of  the  general  process  and  depend  on  the  same 
exciting  cause  as  the  intrapulmonary  change.  Whether  the  fibrous 
hyperplasia  can  begin  in  the  pleura  and  by  extension  inward  along  the 
interlobular  septa  secondarily  involve  the  lung  is  not  clear.     As  can  be 


D.ZCha?! 


Fig.  282. — Fibrosis  of  the  lung  in  which  the  greatly  thickened  pleura  and  the  fibrosis  at  the 
root  of  the  lung  are  independent  of  each  other.      (Phipps  Institute,  Fifth  Report.) 

seen  in  Fig.  284,  the  greatly  thickened  pleura  and  the  fibrosis  at  the  root 
of  the  lung  are  independent  of  each  other,  while  in  Fig.  285  the  thickened 
pleura  and  the  fibrosis  within  the  lung  are  definitely  associated.  It  is 
quite  probable  that  in  some  instances  the  two  processes  are  dependent 
on  the  same  exciting  factor.     Rarely  the  pleura  may  escape  entirely. 

It  is  not  often  that  a  lung  which  has  undergone  fibroid  change  retains 
its  normal  size.  Such  a  lung  is  nearly  always  smaller  than  normal,  the 
reduction  in  size  being,  in  some  instances,  extraordinary.  In  the  variety 
known  as  Corrigan's  cirrhosis  the  lung  may  not  exceed  the  size  of  a 
clenched  fist. 


430         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 


'i 


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Fig.   283. — Reticular  fibrosis.      (Phipps  Institute,  Fifth  Report.) 


:*.,;•. 


ftsfc.      "'•■■ 


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Fig.   284. — Fibrosis  of  the  lung  in  which  the  thickened  pleura  and  the  fibrosis  within  the 
lung  are  definitely  associated.      (Phipps  Institute,  Fifth  Report.) 


DISEASES    OF    THE    LUNGS 


431 


Dilatation  of  the  bronchi  is  pretty  constantly  present  in  extreme 
grades  of  fibrosis.  In  some  instances  the  bronchial  dilatation  is  the 
most  prominent  feature  (see  section  of  Bronchiectasis). 

Fibrosis  of  the  lung  secondary  to  croupous  pneumonia  is  not  com- 
mon.    Occasionally  the  fibrinous  exudate  is  not  removed  and  a  fibrous 


Fig. 


285. — Chronic  fibrosis  of  left  lung.      Marked  retraction  of  left  chest, 
great  vessels  displaced  toward  the  affected  side. 


Heart  and 


hyperplasia  may  start  in  the  septa  and  peribronchial  tissue.  In  fibrosis 
of  this  type  the  lung  is  red  in  color,  tough  and  airless,  and  presents  the 
appearance  of  a  piece  of  muscle.  This  constitutes  what  is  known  as 
carnification  of  the  lung. 


432         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

When  the  fibroid  process  is  tuberculous  in  origin,  apical  cavities  are 
commonly  present  and  the  fibroid  tissue  is  densest  about  the  cavity. 
The  overlying  pleura  also  becomes  greatly  thickened.  Gradually  the 
process  extends  until  the  rest  of  the  lobe  or  entire  lung  is  involved  in 
the  fibroid  change.  In  one  case  at  the  Phipps  Institute  the  enveloping 
layer  of  fibrous  tissue  about  an  apical  cavity  was  at  no  point  less  than  y± 
inch  in  thickness. 

While  the  fibrous  tissue  at  times-becomes  cartilaginous  and  very  hard, 
I  have  never  seen  it  undergo  osseous  changes.  Mangini,1  however,  has 
found  records  in  the  literature  of  twenty-three  cases  of  an  ossifying  process 
ramifying  in  the  lungs.  In  a  case  observed  by  him  bone  needles  could 
be  felt  in  the  lower  lobes  and  cohering  to  form  an  actual  arborization. 
The  process  is  believed  to  result  from  repeated  inflammatory  processes. 

The  heart  is  usually  displaced  toward  the  affected  side  (Fig.  285)  and 
shows  hypertrophy  or  dilatation  of  the  right  ventricle.  The  findings 
in  the  other  organs  do  not  conform  to  any  special  rule.  Frequently 
there  is  evidence  of  arterio-sclerosis,  interstitial  changes  in  the  kidneys, 
and  occasionally  in  the  other  viscera.  This  widespread  sclerosis  in  the 
various  viscera  led  at  one  time  to  the  belief  that  the  pulmonary  fibrosis 
was  simply  a  part  of  a  general  fibroid  diathesis.  Such  a  view  no  longer 
receives  any  support.  The  age  of  the  patients  and  the  congestion  which 
results  from  the  obstruction  offered  to  the  right  heart  are  doubtless  the 
true  causes  of  the  associated  fibrosis. 

Symptoms. — The  clinical  picture  of  massive  fibrosis  due  to  the  tubercle 
bacillus  and  that  which  results  from  a  chronic  inflammatory  condition 
is  identical.  Whether  the  fibrosis  is  due  to  tuberculosis  or  not  in  a  given 
case  must  depend  to  a  great  extent  on  the  examination  of  the  sputum. 
In  the  majority  of  instances  the  patient  is  past  the  middle  period  of  life 
when  first  seen.  While  fibrosis  due  to  the  tubercle  bacillus  is  often  under 
observation  during  the  period  in  which  the  pathological  changes  are 
taking  place,  one  rarely  sees  the  pure  form  of  fibrosis  until  the  process  has 
become  well  established.  Patients  presenting  either  form  of  fibrosis 
give  a  history  of  long-standing  cough,  expectoration,  occasional  attacks 
of  blood  spitting  and  dyspnea  on  exertion.  The  temperature  is  either 
normal  or  shows  only  a  slight  afternoon  rise  (99°F.).  The  pulse  rate  is 
not  accelerated.  In  spite  of  the  long  duration  of  the  disease,  from  five 
to  twenty  years  or  more,  the  general  health  may  be  but  little  impaired. 
The  patient  suffers  no  great  inconvenience,  except  dyspnea  on  exertion 
and  takes  part  in  the  ordinary  affairs  of  life. 

So  long  as  the  cardiac  functions  are  normally  maintained  the  patient 
may  not  consult  a  physician.  When  first  seen  it  is  usually  because  of 
an  attack  of  pleurisy,  of  blood  spitting  or  because  of  increased  cough, 
dyspnea  or  swelling  of  the  feet,  the  latter  symptom  being  indicative  of 
failing  compensation.  The  exceptions  to  this  general  rule  are  the  cases 
in  which  dilatation  of  the  bronchi  is  a  prominent  feature.  If  bronchi- 
ectasis is  present,  the  sputum  is  usually  very  abundant  and  not  infre- 
quently has  a  very  offensive  odor. 

Physical    Signs. — Inspection. — The    affected    side  is    shrunken    and 

motionless  and  the  shoulder  on  this  side  lower  than  its  fellow  (Fig.  285). 

The  intercostal  spaces  are  obliterated,  and  in  some  instances  the  ribs 

overlap.     The  spine  is  bowed  laterally,  the  convexity  being  always  away 

1  Lyon  Medical,  April  26,  1914. 


DISEASES    OF    THE    LUNGS  433 

from  the  affected  side;  the  angle  of  the  scapula  may  be  tipped  back  from 
the  chest  wall.  Litten's  shadow  is  absent  on  the  affected  and  well 
marked  on  the  unaffected  side.  A  fluoroscopic  examination  will  show 
the  diaphragm  to  be  much  flatter  than  normal  on  the  affected  side.  The 
chest  tracing  in  Fig.  286  shows  the  great  disparity  existing  between  the 
two  sides  of  the  chest. 

Displacement  of  the  heart  is  an  almost  constant  feature.  When  the 
left  side  is  affected,  the  heart  is  pulled  upward  and  outward  and  maj- 
be  displaced  to  the  fourth  interspace  in  the  mid-axillary  line.  In  right- 
sided  cases  the  displacement  is  even  more  striking.  Strong  pulsation 
may  be  noted  in  the  fifth  or  sixth  interspace  in  the  right  nipple  line.  It 
is  to  be  borne  in  mind  that  the  pulsation  in  this  situation  is  not  caused 
by  the  apex  but  by  the  body  of  the  heart. 

Top 


Fig.  286.— (A)  Chest  tracing  from  a  case  of  left-sided  fibroid  disease.     (B)  Spinal  deform- 
ity showing  marked  curvature  of  spine  away  from  the  affected  side. 

The  unaffected  side  is  full,  the  interspaces  wide,  and  the  expansion 
free. 

Marked  clubbing  of  the  fingers  and  also  of  the  toes  may  be  present 
if  the  bronchi  are  dilated. 

Palpation. — This  serves  to  verify  the  diminution  of  expansion  and 
the  location  of  the  apex  beat.  Over  the  affected  side  the  tactile  fremitus 
varies;  it  may  be  greatly  diminished  or  it  may  be  exaggerated. 

Percussion. — Over  the  affected  side,  especially  over  the  base  of  the 
lung  the  percussion  note  is  impaired  or  dull.  If  dilatation  of  the  bronchj 
is  a  prominent  feature  a  tympanitic  percussion  note  may  be  elicited  near 
the  angle  of  the  scapula  or  if  the  upper  lobe  is  involved,  beneath  the 
clavicle.  Over  the  unaffected  side  the  note  is  hyperresonant.  Topo- 
graphical percussion  of  the  healthy  lung  will  also  show  that  it  extends 
beyond  the  middle  line  anteriorly  and  that  a  resonant  note  is  obtained 
an  inch  or  more  below  the  normal  base  line  posteriorly. 

Auscultation. — The  breath  sounds  over  that  portion  of  the  lung  which 
has  undergone  fibroid  change  are  often  distant  and  the  expiratory  sound 
may  have  a  prolonged  and  bronchial  quality.  If  the  bronchi  are  dilated, 
amphoric  breathing  and  whispering  pectoriloquy  may  be  heard  near  the 
angle  of  the  scapula.     Rales  may  be  absent.     If  present  they  may  be  of 


434         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

the  fine  cracking  variety  or  they  may  be  wheezing  in  character.  Vocal 
resonance  may  be  diminished  or  exaggerated. 

Diagnosis. — -The  salient  features  of  massive  unilateral  pulmonary 
fibrosis  are:  a  history  of  long-standing  cough,  dyspnea  and  marked 
retraction  of  one  side  of  the  chest  with  displacement  of  the  heart  toward 
the  affected  side.  If  the  lower  lobe  is  involved  and  the  upper  one  is 
relatively  clear,  the  condition,  in  all  probability,  is  not  due  to  tuberculosis. 
When,  however,  the  upper  lobe  is  the  site  of  the  change  and,  in  addition 
the  bronchi  are  dilated,  pure  fibrosis  cannot  be  differentiated  from  that 
due  to  tuberculosis,  without  a  sputum  examination.  The  neglect  of  this 
precaution  leads  to  many  mistakes. 

In  regard  to  pulmonary  fibrosis  and  bronchiectasis  it  is  not  a  question 
of  distinguishing  between  them,  but  of  determining  whether  the  two  con- 
ditions are  associated.  Both  are  due  to  the  same  causes.  In  about  80 
per  cent,  of  the  cases  of  massive  fibrosis  the  bronchi  are  dilated.  Rarely 
the  bronchi  are  dilated  without  associated  interstitial  changes  in  the 
pulmonary  tissue.  If  in  a  case  with  marked  unilateral  retraction  of  the 
chest  wall  there  are  also  present  a  paroxysmal  cough,  profuse  expectora- 
tion, often  of  a  foul  odor,  and  marked  clubbing  of  the  fingers,  it  is  reason- 
ably certain  that  in  addition  to  the  fibroid  changes,  the  bronchi  are  also 
dilated. 

One  of  the  most  frequent  errors  is  that  of  mistaking  a  chronic 
empyema  for  a  chronic  pulmonary  affection.  In  the  early  stages  of  a 
purulent  effusion  the  effected  side  is  usually  fuller  than  the  unaffected 
side.  If  the  empyema  goes  unrecognized,  it  sometimes  undergoes  partial 
absorption.  The  liquid  portion  is  absorbed  leaving  behind  a  putty-like 
mass  made  up  of  pus  cells  and  lymph.  In  addition  the  pleura  becomes 
greatly  thickened.  As  a  result  the  chest  wall  becomes  retracted  and 
eventually  the  lung  itself  undergoes  interstitial  changes.  I  have  already 
alluded  to  the  part  played  by  encysted  empyema  in  the  production  of 
pulmonary  fibrosis. 

Pneumoconiosis 

The  term  pneumoconiosis  (irvevjjioov,  lung;  rj  kovls,  the  dust)  is  applied 
generally  to  pulmonary  affections  which  develop  as  the  result  of  the 
inhalation  of  dust.  "The  term  'dusts'  as  I  would  here  apply  it,  includes 
all  those  fine,  solid  particles  which  are  thrown  off  from  various  substances 
in  the  processes  of  manufacture  or  treatment  of  articles  in  common  use 
in  daily  life,  such  as  earthenware  utensils,  knives,  needles,  or  mechanical 
instruments,  like  files  or  saws;  or  ornamental  things,  such  as  ornaments  of 
pearl,  ivory  or  turned  wood;  or  articles  that  are  worn,  of  silk,  cotton, 
hemp,  fur;  or  things  that  we  use  for  food,  such  as  flour;  or  for  creating 
warmth  such  as  coal;  or  for  using  as  a  supposed  luxury,  such  as  tobacco 
and  snuff."1  From  the  above  description  it  is  seen  that  the  term  pneu- 
moconiosis is  a  very  comprehensive  one.  A  number  of  synonyms  have 
been  used  to  indicate  the  particular  variety  of  dust,  namely,  anthracosis 
or  coal  dust;  chalicosis  or  flint  dust;  siderosis  or  iron  dust;  byssinosis  or 
cotton  dust;  tobacosis,  etc.  In  addition  a  variety  of  popular  names  have 
been  applied  to  the  dust  diseases,  the  terms  used  indicating  the  occupa- 
tion, as  for  example,  miner's  asthma,  grinder's  rot,  potter's  rot,  potter's 

1  Richardson,  Scientific  American  Supplements,  1876. 


DISEASES    OF    THE    LUNGS  435 

asthma.  That  the  prolonged  inhalation  of  dust  is  capable  of  producing 
pathological  changes  in  the  lungs  and  bronchi  has  been  long  known. 
For  the  first  systematic  treatise  on  the  subject  we  are  indebted  to 
Ramazzini  (1703).  During  the  last  century  the  subject  was  thoroughly 
studied,  especially  by  English  physicians,  who  had  unusual  opportunities 
because  of  the  great  diversity  of  manufacturing  processes  in  England  and 
the  large  number  of  people  engaged  in  these  trades.  In  this  country  the 
subject  of  occupational  diseases  has  received  but  scanty  attention  and 
it  is  only  within  the  past  few  years  that  several  of  the  States  have  re- 
quired physicians  to  report  on  their  occurrence. 

Etiology. — The  etiology  of  pneumoconiosis  is  very  complex.  The 
condition  is  caused  by  a  variety  of  dusts,  some  of  which  are  exceedingly 
irritating  and  produce  in  a  relatively  short  time,  marked  damage  to  the 
respiratory  tract;  in  the  case  of  others,  pulmonary  changes  are  produced 
very  slowly  and  the  general  health  remains  unimpaired  for  years.  Fur- 
thermore, individuals  seem  to  vary  in  their  ability  to  withstand  the 
effects  of  the  same  kinds  of  dust.  Some  workers  after  years  of  prolonged 
exposure  show  little  or  no  impairment  of  health  while  others,  at  varying 
periods,  gradually  succumb  to  its  effects.  In  addition  there  are  other 
cooperating  factors,  not  connected  with  the  occupation  itself,  such  as  an 
insanitary  living  environment,  unhygienic  home,  insufficient  food,  and 
intemperance.  This  latter  aspect  of  the  subject  has  been  emphasized 
by  a  number  of  English  writers  on  the  subject.  In  the  case  of  miners 
the  great  depth  at  which  some  of  them  work  may  have  some  influence  in 
bringing  about  respiratory  changes. 

The  extent  to  which  pneumoconiosis  prevails  cannot  be  determined 
as  the  term  is  practically  never  employed  to  indicate  the  cause  of  death 
nor  even  to  indicate  the  nature  of  the  illness  during  life.  How  many 
cases  of  bronchitis,  acute  or  chronic,  of  broncho-pneumonia  or  other  acute 
and  chronic  inflammations  of  the  respiratory  tract  are  produced  as  the 
result  of  the  inhalation  of  dust,  is  therefore  problematical.  The  only 
exception  to  this  is  tuberculosis.  For  many  years  it  has  been  recognized 
that  the  mortality  from  tuberculosis  among  those  working  in  the  dusty 
trades  is  excessive. 

There  are  two  main  types  of  dust:  (1)  the  inorganic,  and  (2)  the 
organic. 

Inorganic  Dust. — This  is  by  far  the  most  harmful  because  of  the 
sharp,  angular  particles  which  produce  harmful  mechanical  injuries  and 
because,  in  some  instances,  injurious  chemical  effects  are  also  produced. 
The  different  forms  of  pneumoconiosis  are  as  follows:  (a)  Anthracosis 
(miner's  asthma,  coal  miner's  phthisis,  black  spit).  This  is  by  far  the 
commonest  form  of  dust  disease  and  the  one  about  which  the  most  has 
been  written.  The  condition  exists  to  some  extent  in  practically  all  who 
have  worked  for  any  length  of  time  in  a  coal  mine.  It  occurs  in  a  more 
severe  form  in  those  who  mine  the  anthracite  or  hard  coal.  This  is  due 
to  the  fact  that  the  bituminous  or  soft  coal  is  not  hard  and  stony  as  the 
anthracite. 

The  lungs  of  practically  all  urban  dwellers  show  some  evidence  of 
anthracosis.  Usually  it  consists  of  nothing  more  than  the  grayish  dis- 
coloration of  the  lungs  common  to  all  who  reach  adult  life  but  in  com- 
munities in  which  the  amount  of  coal  smoke  and  soot  is  excessive  the 
condition  becomes  more  marked  and  may  constitute  a  true  anthracosis. 


436         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Klotz1  in  a  recent  study  has  shown  that  among  those  who  have  lived  for 
years  in  Pittsburgh,  Pa.,  the  amount  of  carbon  deposited  in  the  lungs  is 
excessive  as  shown  both  by  the  residual  ash  and  the  degree  of  pulmonary 
fibrosis  produced. 

Chalicosis  and  Silicosis. — In  these  forms  of  pneumoconiosis  the  dust 
consists  of  sharp  angular  particles  which  give  rise  to  considerable 
mechanical  injury  to  the  mucous  membrane.  Aside  from  dust  which 
contains  poisonous  mineral  substances,  such  as  lead,  that  which  is  com- 
posed of  fine  particles  of  flint  or  silex  is  the  most  dangerous  form 
encountered.  Flint  and  silicious  dust  are  met  with  in  a  variety  of  oc- 
cupations, namely,  potters,  stone  masons,  stone  quarry  workmen,  etc. 


JS*3gE34», 


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W'l*  -*£  $  > 


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Fig.  287.- — Nodular  dissemination  of  anthracosis.     (Klotz,  in  American  Journal  of 

Public  Health.) 

Among  the  gold  miners  of  South  Africa  a  particularly  severe  form  of  in- 
fection occurs  from  exposure  to  dust  composed  of  fine  particles  of  silex. 
The  dust  arises  as  the  result  of  using  machine  rock  drills  (Oliver). 

Siderosis. — This  is  due  to  fine  particles  of  iron  dust.  The  condition 
is  rare.  The  occupations  involved  are  those  in  which  the  red  oxide  of 
iron  is  used.  Looking-glass  makers,  gold  beaters,  and  glass  polishers  are 
among  the  workers  exposed  to  this  form  of  dust.  In  cases  of  this  type 
the  sputum  may  be  reddish  and  at  post-mortem  the  lung  may  present 
a  brick-red  appearance  due  to  the  red  oxide  of  iron.  Among  workers 
who  smooth  or  sharpen  iron  or  steel  implements  on  a  sandstone,  pneu- 

1  Am.  Jour.  Public  Health,  Oct.,  1914. 


DISEASES    OF    THE    LUNGS  437 

moconiosis  is  quite  common.     This  form  is  due,  in  part,  to  fine  particles 
of  metal  and,  in  part,  to  fine  particles  from  the  sandstone. 

Dust  from  Crushed  Slag. — Slag,  a  name  applied  to  the  refuse  from 
blast  furnaces  after  the  iron  has  been  removed,  is  sometimes  finely 
crushed.  In  this  pulverized  form  it  is  used  as  a  fertilizer  because  of  the 
large  quantity  of  phosphate  of  lime  which  it  contains.  This  form  of  dust 
produces  a  curious  infection  of  the  lungs  in  that  it  resembles  acute 
croupous  pneumonia.  This  form  of  infection  will  be  considered  more  in 
detail  under  the  section  on  Morbid  Anatomy. 

Oeganic  Dust. — The  evidence  that  inorganic  dust  is  capable  of 
producing  definite  pathological  changes  in  the  lungs  is  conclusive.  When 
we  come  to  consider  the  effect  of  organic  dust,  however,  we  lack  definite 
proof  that  it  is  of  itself  injurious.  While  it  is  true  that  many  of  the 
occupations  in  which  organic  dust  occurs  are  attended  by  a  high  death 
rate  from  tuberculosis,  it  is  questionable  whether  the  dust  plays  any- 
thing more  than  a  very  minor  role.  Oliver  states  that  if  we  leave  out 
of  consideration  the  moisture  which  has  been  artificially  introduced  in 
the  weaving  sheds,  it  cannot  be  said  that  the  manufacture  of  cotton  is 
per  se  an  unhealthy  occupation.  In  this  country  much  of  the  tubercu- 
losis and  general  ill  health  among  cotton  operatives  can  be  traced  to 
their  deplorable  living  conditions,  and  to  the  fact  that  many  especially 
in  the  South,  enter  the  trade  at  an  early  age. 

In  the  manufacture  of  felt  hats  the  hair  of  rabbits  and  similar  animals 
is  largely  used.  This  occupation  has  been  classed  among  the  dangerous 
dusty  trades.  At  the  Phipps  Institute  it  has  been  our  experience  that 
among  the  hatters  who  applied  for  treatment  all  were  employed  in  the 
molding  room  which  is  wet  and  damp.  Oliver  states  that  he  has  never 
seen  ill  health  among  those  engaged  in  the  handling  of  tobacco,  which 
could  be  attributed  to  the  trade  itself.  In  the  United  States  cigar  makers 
have  a  very  high  mortality  from  tuberculosis.  This  is  due,  in  all  proba- 
bility, to  the  fact  that  the  workers  are  rendered  more  susceptible  to  this 
infection  because  of  a  deterioration  of  health  due  to  nicotine  poisoning. 
Workers  in  this  trade  have  informed  me  that  many  of  them  are  rejected 
for  insurance  because  of  a  "tobacco  heart." 

It  is  my  personal  belief  that  pneumoconiosis  rarely  if  ever  develops 
as  the  result  of  exposure  to  organic  dust.  Not  only  is  this  form  of  dust 
incapable  of  producing  a  mechanical  injury,  but  it  is  doubtful  if  any  of 
it  ever  reaches  the  finer  bronchi  and  lung  cells.  The  vast  majority 
of  the  dust  particles  are  prevented  from  penetrating  very  deeply  into  the 
bronchial  tube  because  of  the  action  of  the  ciliated  epithelium  and  the 
moisture  in  the  larger  tubes.  The  high  incidence  of  tuberculosis  among 
those  exposed  to  this  type  of  dust  is  to  be  explained  in  other  ways, 
namely,  low  wages,  bad  home  environment,  poor  food,  etc. 

During  the  threshing  season  in  the  fall,  it  is  not  uncommon  for  those 
who  are  exposed  to  the  dust  produced  by  the  wheat,  oats,  etc.,  passing 
through  the  threshing  machine,  to  develop  acute  symptoms.  Workers 
who  are  especially  susceptible  will,  in  the  beginning  of  the  threshing 
season,  develop  a  headache  and  great  irritation  of  the  respiratory  tract. 
In  addition  there  is  considerable  depression,  a  sensation  of  chilliness  and 
often  high  fever.  After  a  few  days  these  symptoms  pass  off  and  the 
worker  is  apparently  immunized  for  the  remainder  of  the  season.  These 
symptoms  have  been  attributed  to  a  pollen  infection,  especially  that  of 


438  DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

rag  weed,  and  are  believed  to  be  somewhat  analogous  to  the  autumnal 
form  of  hay  fever.  A  similar  condition  is  encountered  among  those 
engaged  in  the  manufacture  of  shoddy.  During  the  grinding  of  the 
rags  by  machinery  considerable  quantities  of  dust  are  thrown  off,  in- 
halation of  which  is  extremely  trying  to  new  hands  but  which  has  little 
or  no  immediate  effects  on  the  older  work  people.  Those  persons  who 
are  new  to  the  trade  develop  what  is  known  as  "shoddy  fever,"  the  symp- 
toms of  which  are  a  rise  of  temperature,  severe  headache,  signs  of  bron- 
chial catarrh,  and  running  at  the  nose.  The  work  people  shiver  as  if 
they  were  going  to  have  a  severe  fever,  and  they  complain  of  muscular 
pains  (Oliver). 

Pneumoconiosis  and  Its  Relation  to  Tuberculosis. — The  relationship 
which  exists  between  the  inhalation  of  dust  and  tuberculosis  is  an  inter- 
esting one,  and  the  belief  that  dust  has  a  strong  predisposing  effect  in 
producing  pulmonary  tuberculosis  is  quite  generally  accepted.  When 
we  recall,  however,  the  changes  which  are  produced  in  the  lung  by  reason 
of  the  inhalation  of  inorganic  dust,  it  is  evident  that  the  process  is  in  the 
beginning,  a  non-tuberculous  fibrosis  of  the  lungs.  Furthermore,  it  is 
well  known  that  the  symptoms  and  physical  signs  produced  by  such 
changes  often  simulate  those  produced  by  tuberculosis  very  closely. 
It  seems  quite  likely,  therefore,  that  in  not  a  few  instances  it  has  been 
assumed  that  the  process  was  tuberculous,  and  death  was  ascribed  to 
this  cause,  without  an  examination  of  the  sputum  having  been  made  to 
determine  the  true  nature  of  the  disorder.  Tatham1  in  commenting 
on  this  aspect  of  the  question  states  that:  "Potters  succumb  to  non- 
tubercular  disease  of  the  lungs  much  more  rapidly  than  they  do  to 
tubercular  phthisis,  and  it  is  certain  that  much  of  the  so-called  potter's 
phthisis  ought  properly  to  be  termed  cirrhosis  of  the  lung.  Deaths  from 
this  affection  should  never  be  included  under  the  head  of  phthisis,  which 
term  is  now  restricted  by  universal  consent  to  the  tubercular  malady 
of  that  name." 

On  the  other  hand,  it  is  to  be  borne  in  mind  that  the  cause  of  death 
in  cases  of  this  type  is  not  infrequently  given  as  being  due  to  chronic 
bronchitis,  emphysema,  pleurisy,  etc.  This  might  possibly  equalize  the 
error. 

There  is  still  another  factor  to  be  considered,  namely,  the  effect  of 
an  antecedent  fibrosis  of  the  lungs.  It  is  well  known  that  the  stimula- 
tion of  connective-tissue  growth  is  the  way  in  which  nature  overcomes 
tuberculosis.  Therefore,  anything  which  stimulates  such  a  growth  in 
the  lungs  should  aid  in  preventing  the  tubercle  bacilli  from  getting  a 
foothold,  or  in  overcoming  or  retarding  their  growth,  if  they  become 
established  in  the  pulmonary  tissue.  This  is  the  view  held  by  Wain- 
wright  and  Nichols,  who  found  that  true  tuberculosis  was  not  a  frequent 
finding  among  coal  miners,  but  that  extensive  fibroid  changes  in  the 
lungs,  as  the  result  of  coal  dust,  was  exceedingly  common.  The  protect- 
ing influence,  in  their  opinion,  was  the  fibroid  tissue  and  not  the  coal  dust 
itself,  the  latter  having  been  held  by  some  to  have  germicidal  qualities. 

While  potters,  for  instance,  are  not  freed  from  the  danger  of  becoming 

tuberculous  by  reason  of  the  fibrosis  which  is  produced  incidental  to  the 

inhalation  of  clay  and  flint  dust,  it  seems  reasonably  certain  that  the 

fibrosis  does  tend  to  retard  the  progress  of  the  tuberculous  infection. 

1  Oliver's  "Dangerous  Trades." 


DISEASES    OF   THE    LUNGS  439 

Thus  it  has  long  been  recognized  that  the  age  period  at  which  potters 
succumb  to  tuberculosis,  if  it  does  develop,  is  far  beyond  the  average, 
and  in  addition,  so  far  as  my  observation  goes,  the  disease  seems  to  be 
much  less  severe  than  the  same  amount  of  damage  produced  in  other 
classes  of  patients. 

Morbid  Anatomy. — While  all  forms  of  inorganic  dust  bring  about 
essentially  the  same  changes  in  the  respiratory  tract,  they  vary,  one  from 
another,  in  the  extent  of  the  lesions  produced  and  the  severity  of  the 
symptoms.  The  sharper  and  more  angular  the  dust  particles,  the  greater 
will  be  the  amount  of  mechanical  injury  and  hence  the  greater  the 
inflammatory  reaction. 

The  least  dangerous  of  the  inorganic  dusts  is  that  arising  from  coal, 
especially  the  soft  or  bituminous  variety.  It  is  this  form  of  pneumoconio- 
sis that  has  been  most  thoroughly  studied.  At  the  present  time,  it  is 
pretty  generally  agreed  that  pneumoconiosis  is  the  result  of  dust  taken 
into  the  lungs  during  the  inspiratory  act.  The  view  that  the  dust  is 
conveyed  to  the  lungs  by  way  of  the  lymphatics  after  having  been  swal- 
lowed, is  of  little  importance,  as  far  as  this  type  of  infection  is  concerned. 

Exposure  to  almost  any  kind  of  dust,  even  for  a  short  time,  is  apt  to 
irritate  the  upper  respiratory  tract  and  produce  coughing.  If  the  exposure 
is  sufficiently  long  there  develops  a  pharyngitis  and  later  a  bronchitis. 
Between  simple  irritation  as  the  result  of  a  brief  exposure,  and  extensive 
tissue  changes,  as  the  result  of  prolonged  exposure,  varying  degrees  of 
pathological  alteration  may  occur. 

Clay  and  flint  both  contain  very  hard,  sharp,  angular  particles  of 
silex,  which  when  drawn  into  the  respiratory  tract  during  inhalation  are 
not  dissolved  by  the  bronchial  secretions,  but  are  deposited  in  the  alveoli 
and  smaller  bronchi.  For  a  varying  length  of  time  the  inhaled  dust  is 
arrested  in  its  advance  by  the  mucous  secretion  in  the  bronchi,  by  the 
ciliated  epithelium  lining  the  tubes  and  by  the  action  of  the  phagocytes. 
Sooner  or  later,  however,  these  defensive  forces  weaken,  and  finally  the 
dust  passes  into  the  lymph  channels,  and  also  along  the  finer  bronchi, 
until  it  reaches  the  parenchyma  of  the  lungs.  As  a  foreign  substance  it 
then  sets  up  a  chronic  inflammatory  process.  The  initial  deposits  of 
dust  occur  for  the  most  part  in  the  posterior  and  inferior  portions  of  the 
lungs. 

Microscopial  Changes. — The  gradual  evolution  of  anthracosis  has 
been  described  by  Wainwright  and  Nichols,1  Haythorn2  and  Klotz3 
to  whom  I  am  indebted  for  most  of  the  following  description. 

1.  In  the  case  of  those  who  have  worked  in  a  coal  mine  but  a  few 
months  some  of  the  epithelial  cells  lining  the  alveoli  become  swollen  and 
contain  particles  of  coal  dust.  Sometimes  a  few  larger  desquam- 
ated cells  containing  much  pigment  are  found  in  the  alveola?  lying  loose 
with  some  detritus  and  free  dust  particles.  Even  in  the  early  stage, 
dust  particles  are  seen  in  the  walls  of  the  air  vesicles  and  around  the 
small  bronchi.  In  this  stage  there  is  no  evidence  of  connective-tissue 
proliferation. 

2.  In  those  who  have  worked  in  the  mines  for  several  years  the  swollen 
cells  containing  dust  particles  are  much  more  numerous  and  in  addition 

1  Am.  Jour.  Med.  Sc.,  1905,  vol.  cxxx. 

2  Jour.  Med.  Res.,  December,  1913. 

3  Am.  Jour.  Public  Health,  vol.  iv,  No.  10. 


440         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA.    AND    DIAPHRAGM 

there  are  present  large  mononuclear  phagocytes  filled  with  carbon  particles. 
These  pigment-bearing  phagocytes  are  also  found  in  the  interalveolar 
lymph  spaces,  in  the  lymphatics  of  the  interlobular  septa,  in  those  about 
the  vessels,  and  beneath  the  pleura  and  in  the  lower  layer  of  the  bronchial 
mucosa. 

As  the  accumulations  of  pigment  gradually  increase,  they  not  only 
form  lines  along  the  septa  of  the  lobules  and  the  vascular  channels,  but 
nodular  collections  appear  at  the  points  of  junction  of  the  various  lymph 
channels  where  small  receptaculi  are  formed.  These  nodules  become  so 
prominent  that  they  are  readily  felt  by  the  finger,  and  at  times  the  course 
of  the  lymph  channel  can  be  detected  by  the  sensation  of  touch  (Fig. 
287). 

At  the  points  where  the  dust  collects  the  fibrous  tissue  is  arranged  in 
concentric  layers,  so  as  to  form  small  nodules.  Between  the  layers  of 
fibrous  tissue  and  especially  toward  the  periphery,  the  particles  of  carbon 
are  especially  numerous.  The  fibrous  masses  are  well  seen  in  the  septa 
that  run  in  from  the  pleura.  In  places  considerable-sized  black  triangles 
with  their  bases  on  the  pleura  are  seen,  showing  where  the  septum  has 
been  completely  filled  up  with  dust.  The  striking  point  in  the  whole 
picture  is  the  extensive  plugging  and  obliteration  of  the  small  and 
medium-sized  lymphatics  and  the  compression  of  the  large  ones.  In  the 
pleura  and  the  peribronchial  lymph  nodes  the  picture  is  a  similar  one 
(Haythorn).  In  this  stage  the  bronchial  and  mediastinal  lymph  nodes 
become  enlarged.  As  the  result  of  exposure  to  nearly  any  kind  of  dust 
the  bronchial  lymph  nodes  become  black,  in  the  case  of  coal  miners,  in- 
tensely so. 

3.  The  third  change  noted  by  Wainwright  and  Nichols  is  important 
from  the  standpoint  of  prevention.  They  found  that  in  the  case  of 
individuals  who  had  formerly  been  miners,  but  who  for  many  years  had 
not  followed  that  occupation,  the  lungs  no  longer  showed  signs  of  irrita- 
tion. The  swollen  epithelium  had  subsided  and  again  become  normal, 
and  neither  the  cells  nor  the  alveoli  contained  dust.  The  deposits  of 
dust  in  the  alveolar  walls,  the  septa  and  peribronchial  tissue,  however, 
still  remained,  as  did  also  the  connective-tissue  thickening. 

Macroscopic  Changes. — There  is  usually  some  evidence  of  emphysema. 
This  may  be  extensive  or  it  may  be  limited  to  patches  along  the  margins 
or  scattered  through  the  body  of  the  lung. 

In  cases  where  the  exposure  to  dust  has  been  a  matter  of  years,  the 
lung  is  hard  and  more  or  less  solid  as  the  result  of  fibrosis.  The  dominant 
feature  of  pneumoconiosis  is  the  fibrosis.  The  fibroid  changes  are  diffuse 
and  bilateral  (Fig.  288)  but  at  times  a  portion  of  one  lung  or  the  entire 
organ  may  become  densely  fibroid.  The  organ  often  cuts  with  some 
difficulty  owing  to  the  presence  of  gritty,  fibrous  nodules.  The  cut  sur- 
face may  be  smooth  but  usually  has  a  gritty  feel  on  section.  In  the  case 
of  anthracosis  the  cut  surface  exudes  a  black,  ink-like  fluid  (Fig.  289). 
In  this  form  of  fibrosis  of  the  lungs  the  walls  of  the  bronchi  are  often 
thickened  and  cylindrical  dilatation  of  the  bronchial  tubes  is  also  com- 
monly present. 

The  pleural  surfaces  are  usually  adherent,  especially  at  the  bases  of 
the  lungs. 

The  association  of  tuberculosis  and  pneumoconiosis  has  already  been 
considered. 


DISEASES    OF   THE    LUNGS 


441 


The  changes  as  described  above  are,  for  the  most  part,  common  to 
all  forms  of  pneumoconiosis  due  to  inorganic  dust.  The  changes  pro- 
duced in  the  lungs"  of  the  gold  miners  of  South  Africa  and  in  those  exposed 
to  slag  dust  are  worthy  of  special  mention.  According  to  Oliver,  gold 
miners'  'phthisis  is  especially  rapid  in  its  development.  Gold  miners  on 
the  Rand  can  follow  the  employment  but  for  a  few  years;  as  a  rule  from 
five  to  ten  years.  Besides  being  produced  in  a  relatively  short  time,  the 
fibrosis  is  very  extensive  and  gives  rise  to  the  most  extreme  dyspnea. 


Fig.  288. — Diffuse  fibrosis  of  both  lungs,  more  marked  on  left  side.  Bronchiectasis  at 
both  apices  and  some  emphysema  at  right  base.  From  a  male,  age  55,  employed  as  a  potter 
for  45  years.  Exposed  to  clay  dust.  Principal  symptoms:  cough,  expectoration  and  dys- 
pnoea. Sputum  examinations  repeatedly  negative  for  tubercle  bacilli.  Physical  signs  iden- 
tical with  those  encountered  in  advanced  tuberculosis.    (Radiographed by  Dr.  H.  K.  Pancoast.) 


The  disease  is  brought  about  by  the  inhalation  of  a  very  fine  form  of  dust 
composed  of  sharp-pointed  particles  of  silex.  This  dust  is  produced  by 
drilling  the  rock  with  machine  drills.  The  tendency  to  respiratory 
disorders  is  also  increased  by  reason  of  the  fact  that  the  men  are  rapidly 
transported  from  a  warm,  deep  mine  to  the  surface  where  the  air  is  cold. 
In  spite  of  the  evidence  of  extensive  pulmonary  changes  Oliver  was  struck 
by  the  fact  that  these  men  presented  a  healtlry,  bronzed  appearance. 
Although  those  exposed  to  slag  dust  frequently  develop  pulmonary 
disease,  the  changes  in  the  lungs  are  very  different  from  that  ordinarily 
encountered  in  pneumoconiosis.     The  slag  dust  gives  rise  to  an  acute 


442         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

inflammation  of  the  lower  lobe  of  one  of  the  lungs,  which  after  death  is 
found  to  be  the  seat  of  ordinary  gray  hepatization.  "It  is  noteworthy 
that  the  inflammation  of  the  lungs  commences  like  pneumonia  and 
runs  a  similar  course,  with  rigor,  pain  in  the  chest,  rusty  sputa,  and,  in 


Fig.  289. — Anthracosis. 

30  per  cent,  of  the  cases,  herpes  on  the  lips.     On  physical  examination 
signs  of  pulmonary  consolidation  are  to  be  noted"  (Oliver). 

Symptoms. — Exposure  to  any  form  of  dust,  even  for  a  brief  period 
of  time,  is  apt  to  cause  considerable  irritation  of  the  upper  air  passages, 
as  manifested  by  cough  and  sometimes  sneezing.     Owing  to   the  fact 


DISEASES    OF    THE    LUNGS  443 

that  coal  dust  is  relatively  the  least  dangerous  of  the  inorganic  dusts, 
years  may  elapse  before  symptoms  arise  which  are  indicative  of  serious 
pulmonary  damage.  Among  potters,  serious  symptoms  rarely  arise 
until  the  worker  has  been  in  the  trade  from  ten  to  twenty  years.  Accord- 
ing to  Oliver  the  "gold  miner's  phthisis"  of  South  Africa  is  the  most 
serious  of  the  dust  infections  as  the  average  time  the  occupation  can  be 
followed  is  six  and  a  half  years. 

In  the  dusty  trades  little  or  no  inconvenience  is  experienced,  in  the 
beginning,  from  the  inhalation  of  dust.  As  a  rule,  the  first  thing  to  be 
noticed  is  a  slight  irritation  in,  and  a  desire  to  clear,  the  throat.  Next, 
a  slight  cough  develops  which  may  occur  in  the  morning  only.  Later 
some  blackish,  viscid  mucus  appears  after  the  cough.  As  the  process 
advances,  the  cough  and  expectoration  become  more  and  more  marked. 

At  some  period,  varying  with  the  character  of  the  dust,  the  worker 
begins  to  experience  some  tightness  in  the  chest,  the  breathing  gets 
shorter  and  shorter  and  finally  the  disturbed  lung  function  becomes  so 
pronounced  as  to  render  the  victim  less  and  less  capable  of  exertion.  In 
spite  of  this  condition,  however,  the  general  health  may  be  but  little 
impaired,  and  unless  the  dyspnea  be  too  great,  the  patient  may  not  be 
compelled  to  cease  work.  As  time  goes  on  the  sputum  which  at  first  is 
mucoid  in  character,  becomes  mucopurulent  and  blood-streaked  or  even 
a  frank  hemoptysis  may  occur. 

Even  when  the  fibroid  changes  have  become  marked,  the  physical 
signs  may  indicate  nothing  more  than  a  diffuse  bronchitis.  There  is 
quite  likely  to  be  added  to  the  picture,  however,  evidences  of  bron- 
chiectasis. Marked  clubbing  of  the  fingers  and  the  expectoration  of 
large  quantities  of  sputum,  sometimes  of  a  foul  odor,  are  strongly  sug- 
gestive of  an  associated  dilatation  of  the  bronchi. 

If  the  condition  becomes  complicated  with  tuberculosis,  there  is 
little  to  distinguish  the  two  conditions  so  far  as  the  physical  signs  are 
concerned.  The  constitutional  symptoms,  however,  may  become  marked : 
there  may  be  fever,  a  rapid  pulse,  night  sweats,  emaciation,  and  most  im- 
portant of  all,  tubercle  bacilli  are  present  in  the  sputum. 

The  distinguishing  feature  of  general  fibrosis  of  •  the  lungs  is  the 
contrast  between  the  extensive  pulmonary  lesions  and  the  absence  of 
marked  constitutional  symptoms.  "Herein  fibroid  phthisis  presents  a 
well-marked  difference  from  pulmonary  tuberculosis;  and  even  if,  as 
we  have  said,  the  disease  becomes  complicated  with  tubercle,  yet  the 
rate  of  progress  may  be  determined  rather  by  the  character  of  the  pri- 
mary than  of  the  secondary  disease,  though  usually  the  supervention  of 
tubercle  hastens  the  sufferer  into  a  more  rapid  consumption."1 

Physical  Signs. — The  physical  findings  in  cases  of  pneumoconiosis 
are  most  varied,  depending,  as  they  do,  upon  the  stage  of  the  disease 
and  whether  it  is  complicated  or  not.  In  the  early  stages  of  the  process 
examination  of  chest  may  reveal  nothing  unusual,  or,  at  most,  the  signs 
indicative  of  a  bronchitis.  As  the  fibrosis  increases,  however,  abnor- 
malities are  more  and  more  frequently  found. 

Inspection. — When  the  disease  becomes  fully  established  it  will  be 
noted  on  inspection  that  expansion  of  the  lungs  is  deficient;  usually  this 
is  more  marked  on  one  side.     If  the  disease  is  more  marked  on  one  side 

1  Report  of  British  Departmental  Committee  on  Compensation  for  Industrial 
Diseases,  1906,  p.  13. 


444         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

than  the  other,  there  is  also  apt  to  be  some  retraction  of  the  chest  wall. 
Evidences  of  poor  expansion  and  retraction  may  be  present  at  the  apices 
or  at  the  bases,  usually  the  latter.  When  the  left  lung  is  involved, 
the  heart  is  drawn  to  that  side  and,  in  addition,  the  area  of  cardiac 
impulse  may  be  increased  by  reason  of  the  retraction  of  the  lung.  Ex- 
tensive fibrosis  of  the  right  lung  will  cause  the  heart  to  be  drawn  to  the 
right.  Distention  of  the  veins  in  the  neck  may  occur  as  the  result  of 
dilatation  of  the  right  heart. 

The  chest  may  be  of  the  emphysematous  type  but  as  a  rule  the  em- 
physema is  not  sufficiently  marked  to  bring  about  this  change. 

As  the  result  of  an  associated  dilatation  of  the  bronchi  the  fingers  may 
be  markedly  clubbed. 

Palpation. — This  will  aid  in  determining  the  areas  of  deficient  expan- 
sion, the  location  of  the  apex  beat  of  the  heart  and  the  positions  of  the 
lungs  which  have  become  solidified. 

Percussion. — -In  the  beginning  the  percussion  note  is  normal.  If 
emphysema  plays  a  prominent  part  the  note  will  be  hyperresonant.  In 
the  majority  of  instances  the  percussion  note  becomes  impaired  or  nearly 
dull  in  certain  areas,  namely,  the  apices,  the  bases  or  the  interscapular 
regions.  The  dull  areas  may  be  bilateral  or  unilateral.  If  bronchiectasis 
supervenes,  a  tympanitic  note  may  be  obtained.  The  common  sites  for 
noting  this  change  are  either  beneath  the  clavicle  or  near  the  angle  of  the 
scapula. 

Auscultation.- — The  auscultatory  signs  are  numerous  and  varied. 
In  the  formative  stages  of  pneumoconiosis  nothing  abnormal  is  detected. 
As  the  exposure  to  the  dust  becomes  more  prolonged  rales,  both  large  and 
small,  may  be  heard  in  both  lungs.  At  this  time  the  breath  sounds  may 
resemble  those  encountered  in  emphysema,  namely,  a  rather  feeble 
respiratory  murmur  with  prolongation  of  expiration. 

When  the  fibrosis  becomes  at  all  marked  there  are  apt  to  be  certain 
areas  over  which  the  breathing  is  suppressed  and  broncho-vesicular.  Fine 
crackling  rales  are  also  present  at  these  points  and  the  voice  sounds  are 
exaggerated.  Attacks  of  pleurisy  are  not  uncommon  so  that  a  friction 
rub  may  be  noted.  When  the  fibrosis  is  diffuse  and  there  are  no  localizing 
signs,  the  breath  sounds  over  the  lungs  may  be  slightly  harsh  and 
broncho-vesicular  in  character.  Rales  are  usually  constantly  present 
but  at  times  are  more  marked  than  at  others  as  intercurrent  "colds" 
are  quite  common. 

If  the  dilatation  of  the  bronchi  becomes  at  all  marked,  cavity  signs 
(whispering  pectoriloquy,  cavernous  breathing,  metallic  or  resonating 
rales)  are  obtained.  The  cavity  signs  may  be  detected  at  the  apices  or 
the  bases  of  the  lungs.  When  heard  about  the  angle  of  the  scapula, 
they  are  always  suggestive  of  bronchiectasis;  at  the  apices  they  may  be 
due  to  an  excavation,  the  result  of  tuberculosis  or  dilated  bronchi. 

The  heart,  as  a  rule,  presents  nothing  characteristic  of  pneumoconiosis. 

Diagnosis. — An  individual  suffering  from  pathological  changes  in 
the  lungs  as  the  result  of  exposure  to  dust  almost  invariably  seeks  relief 
because  of  shortness  of  breath,  cough  and  expectoration  or  a  gradual 
failure  in  strength.  The  clinical  picture  is  that  of  chronic  bronchitis, 
emphysema  and  asthma,  bronchiectasis  or  last,  but  most  important, 
tuberculosis.  The  recognition  of  pneumoconiosis  depends,  for  the  most 
part,  on  a  knowledge  of  the  occupation  of  the  patient.     If  the  history 


DISEASES    OF    THE    LUNGS  445 

indicates  that  there  has  been  prolonged  exposure  to  an  irritating  form  of 
inorganic  dust  it  is  almost  certain  that  the  symptoms  and  physical  signs, 
no  matter  how  varied  they  may  be,  have  had  their  origin  in  this  way.  A 
knowledge  of  the  role  played  by  dust  is  important,  because  the  process  in 
the  lung  can  be  arrested  if  the  individual  seeks  a  dust-free  occupation. 
Pure  pneumoconiosis  can  be  distinguished  from  that  with  a  com- 
plicating tuberculosis,  only  by  means  of  a  sputum  examination. 

Atelectasis 

By  atelectasis  (dreXrjs,  incomplete;  exrd<ns,  expansion)  is  understood 
the  return  of  lung  tissue,  once  expanded,  to  a  retracted,  airless  state.  The 
terms  collapse  of  the  lungs,  etat  fetal,  and  apneumatosis  are  sometimes 
employed  to  convey  the  same  meaning. 

Etiology. — Atelectasis  may  be  (1)  congenital  or  (2)  acquired. 

1.  Up  to  the  moment  of  birth  the  lungs  are  solid  organs,  the  alveolar 
walls  lying  in  close  contact.  With  the  first  inspiration  the  lungs  undergo 
partial  expansion,  the  alveolar  walls  being  separated  and  the  bronchioles 
assume  their  permanent  shape.  If  the  child  has  not  breathed  at  all, 
the  lungs  present  throughout  the  color  and  texture  of  the  adult  liver. 
If  a  few  respirations  have  occurred,  the  surface  of  the  lung  is  studded 
with  distended  air  vesicles  while  the  remainder  presents  the  appearance 
of  atelectasis.  Congenital  atelectasis  is  met  with  in  still-born  children 
at  term,  in  prematurely  born  children  and  is  often  seen  in  those  with 
congenital  syphilis,  lesions  of  the  central  nervous  system  or  as  the  result 
of  obstruction  of  the  bronchi  by  foreign  bodies  or  secretions.  In  weakly 
children  it  is  probable  that  portions  of  the  lungs  remain  unexpanded 
during  the  first  year  of  life. 

Congenital  atelectasis  is  chiefly  of  medico-legal  interest. 

2.  Acquired  atelectasis  may  arise  as  the  result  of  (a)  interference  with 
the  respiratory  function  within  the  lung  itself  and  (b)  external  mechanical 
pressure. 

(a)  Interference  with  the  respiratory  function  may  be  brought  about, 
by  obstruction  in  the  upper  air  passages  due  to  enlarged  tonsils,  a  denoids 
or  laryngeal  stenosis. 

Another  cause  of  atelectasis  is  obstruction  of  the  bronchi.  This 
may  be  brought  about  by  inflammatory  swelling  of  the  bronchial  mucous 
membrane  and  the  accumulation  of  secretions  within  the  tubes  in  such 
conditions  as  bronchitis,  broncho-pneumonia  and  whooping  cough. 
The  bronchi  may  be  occluded  also  as  the  result  of  a  foreign  body  or  by 
pressure  from  without  by  an  aneurism  or  mediastinal  growth. 

Finally  a  very  common  form  of  atelectasis,  due  to  interference  with 
the  respiratory  function,  is  met  with  in  cachectic  or  moribund  individuals. 
In  such  cases  the  weakening  of  certain  groups  of  muscles  concerned  in 
respiration  fails  to  support  the  chest  wall.  As  a  result  the  cavity  of  the 
thorax  which  should  be  enlarged  by  the  descent  of  the  diaphragm  becomes 
narrowed  and  the  intercostal  spaces  and  lower  parts  of  the  chest  recede 
during  inspiration  thus  causing  the  underlying  parts  of  the  lungs  to 
collapse.  In  conditions  characterized  by  extreme  weakness  whether 
from  old  age,  prolonged  fever,  or  other  cause,  small  areas,  partially  or 
completely  collapsed,  chiefly  at  the  margins  and  bases  of  the  lungs,  are 
of  frequent  occurrence. 


446  DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

A  long  continuance  of  the  above  causes,  especially  when  due  to  enlarged 
tonsils,  adenoids  or  weak  muscles,  may  lead  to  permanent  deformity  of 
the  chest  such  as  the  "  pigeon  breast "  or  the  development  of  marked  lateral 
depressions  (Harrison's  furrow). 

(6)  The  lung  may  be  compressed  by  external  pressure.  The  pressure 
may  be  brought  about  as  the  result  of  a  pleural  effusion,  pneumothorax 
(spontaneous  or  artificial),  aneurism,  tumor,  cardiac  hypertrophy,  peri- 
cardial effusion,  thickening  and  contraction  of  the  pleura  and  by  spinal 
deformities  (see  Figs.  103,  105,  107,  109).  All  of  these  causes  operate 
not  only  by  direct  pressure  but  also  by  interfering  with  the  proper  respir- 
atory movements.  Pasteur1  has  drawn  attention  to  collapse  of  one  of 
the  lower  lobes  due  to  reflex  inhibition  of  the  diaphragm.  This  condi- 
tion is  sometimes  encountered  after  abdominal  operations. 

Morbid  Anatomy. — Atelectasis  may  affect  one  or  both  lungs.  It  may 
be  limited  to  small  circumscribed  areas  or  it  may  involve  an  entire  lung 
or  any  portion  thereof.  When  occurring  in  the  circumscribed  form,  the 
collapse  areas  are  usually  to  be  found  in  those  parts  of  the  lung  where  the 
expansile  power  of  the  chest  is  least,  and  which  are  the  earliest  to  be 
affected  by  muscular  weakness.  Hence,  atelectasis  is  most  commonly 
found  at  the  bases  and  along  the  free  margins  of  the  lungs.  The  middle  lobe 
of  the  right  lung  is  frequently  involved.  In  the  lobular  form,  if  situated 
at  the  periphery  of  the  lung,  the  involved  area  is  sharply  defined,  shrunken, 
depressed  below  the  surface  and  of  a  dark  violet  tint.  On  section  it  is 
smooth  and  glistening  in  appearance  and  on  pressure  a  small  amount  of 
serum  exudes.  The  tissue  not  only  feels  airless  but  also  sinks  when 
placed  in  water.  In  the  early  stages  the  surrounding  lung  tissue  may  be 
edematous;  later  it  usually  undergoes  emphysematous  changes.  If  not 
of  long  standing,  the  collapse  cells  may  become  reinflated.  If,  however, 
they  remain  permanently  collapsed,  interstitial  changes  usually  take 
place. 

When  the  lung  as  a  whole  becomes  collapsed  from  pressure  without, 
as  in  the  case  of  a  pleural  effusion,  pneumothorax,  etc.,  the  organ  is 
greatly  reduced  in  size  and  lies  high  up  in  the  thoracic  cavity  close  to  the 
spinal  column  (see  Fig.  325).  The  lung  has  a  leathery  feel,  the  surface 
is  thrown  into  fine  wrinkles  and  is  of  a  purplish  or  brownish-red  color.  If 
the  pressure  is  marked,  the  organ  becomes  ischemic  and  of  a  grayish  or 
slaty  color.  On  section  the  tissue  resembles  flesh,  does  not  crepitate  and 
sinks  in  water.  Providing  the  pressure  has  not  existed  for  too  long  a 
time  the  lung  will  gradually  reexpand.  If,  however,  the  collapse  has  been 
of  long  standing  the  lung  gradually  undergoes  interstitial  changes  and 
finally  is  transformed  into  a  fibrous  mass  with  or  without  dilatation  of  the 
bronchi.  In  the  early  stages  of  collapse  the  interference  with  the  blood 
supply  renders  the  lung  susceptible  to  infections  such  as  bronchitis  or 
broncho-pneumonia. 

Massive  collapse  of  one  of  the  lower  lobes  as  a  sequel  to  abdominal 
operations  is  clue  to  paralysis  of  the  diaphragm  (see  p.  584).  Pasteur 
states  that  the  deflation  may  be  so  complete  that  the  affected  portion 
sinks  in  water.  In  most  instances  this  form  of  collapse  is  of  brief  duration, 
the  lung  becoming  reexpanded  in  a  day  or  so. 

Symptoms. — Pulmonary  atelectasis  may  occur  without  any  clinical 
manifestations  whatever.  When  present,  symptoms  indicative  of  pulmo- 
1  Annual  Oration,  Med.  Soc,  London,  May,  1911. 


DISEASES    OF    THE    LUNGS  447 

nary  collapse  are  extremely  variable  and  depend  in  great  measure  on  its 
extent  and  on  the  acuteness  and  rapidity  of  its  production.  Thus  collapse 
of  the  lung  may  be  attended  by  sudden  and  alarming  symptoms  as  in 
cases  of  spontaneous  pneumothorax  or  it  may  show  itself  only  by  slight 
shortness  of  breath  on  exertion  as  in  cases  of  pleural  effusion.  In  the 
great  majority  of  instances  in  which  pulmonary  atelectasis  is  present 
the  phenomena  produced  by  this  condition  form  a  part  of  the  clinical 
picture  of  other  well-recognized  disorders. 

Complete  bilateral  atelectasis  is  seen  in  still-born  children  only.  The 
condition  is  of  great  medico-legal  interest  as  it  proves  that  death  occurred 
prior  to  birth. 

In  prematurely  born  children  and  in  those  enfeebled  by  some  con- 
stitutional taint  such  as  syphilis,  the  lungs  may  become  partially  ex- 
panded. In  such  children  the  temperature  is  low  and  the  respirations 
are  rapid  and  superficial.  The  face  is  pallid  and  pinched,  the  lips  and 
hands  cyanosed  and  the  eyes  and  fontanelles  are  sunken.  General 
weakness  is  very  marked  and  the  child  has  difficulty  in  suckling.  As 
a  rule,  this  condition  lasts  for  a  few  days  when  the  cyanosis  becomes  more 
marked,  the  child  lies  in  a  somnolent  state  and  finally  develops  twitching 
or  convulsive  movements  of  the  extremities.  While  the  duration  of 
life  in  these  children  is  usually  but  a  few  days,  death  may  not  occur  for 
several  weeks.  If  the  cyanosis  is  marked,  the  child  rarely  lives  more 
than  a  few  days. 

When  collapse  of  portions  of  the  lungs  occurs  as  a  complication  of 
bronchitis,  broncho-pneumonia,  whooping  cough  or  any  condition 
attended  by  blocking  of  the  smaller  bronchi,  its  presence  is  to  be  inferred 
largely  by  an  increase  in  the  severity  of  symptoms.  As  a  complica- 
tion of  broncho-pneumonia  the  onset  may  be  sudden  and  severe.  There 
is  an  urgent  sense  of  dyspnea  and  respiratory  distress,  the  respiratory 
and  pulse  rates  become  rapid,  the  movement  of  the  alse  nasi  exaggerated, 
and  the  child  becomes  restless  and  fretful.  The  cough  may  be  ineffectual 
due  to  imperfect  inspiratory  expansion  or  it  may  be  violent  and  paroxys- 
mal in  character.  Gradually  the  child  becomes  more  and  more  cyanosed, 
sweats  profusely  and  sinks  into  unconsciousness  or  dies  during  or  after 
a  paroxysm  of  coughing. 

Pulmonary  collapse  which  occurs  as  the  result  of  pressure  exerted  by 
a  pleural  effusion,  tumor,  aneurism,  etc.,  is  rarely  attended  by  marked 
symptoms.  As  a  rule  the  condition  has  been  brought  about  so  gradually 
that  the  opposite  lung  has  had  time  to  accommodate  itself  to  the  change. 
If,  however,  a  pleural  effusion  develops  rapidly  or  entirely  fills  one  side 
of  the  chest,  there  is  dyspnea,  especially  on  exertion,  and  a  sense  of 
oppression. 

The  most  obvious  form  of  atelectasis  is  that  which  occurs  as  the  result 
of  pneumothorax.  While  it  is  true  that  pneumothorax  sometimes 
develops  gradually  and  produces  no  symptoms  the  majority  of  cases  are 
characterized  by  a  sudden  onset.  In  such  instances  the  lung  collapses 
so  suddenly  that  the  intact  lung  has  thrust  upon  it,  without  a  moment's 
warning,  the  entire  burden  of  the  respiratory  function.  The  sudden 
displacement  of  the  heart  and  great  vessels  and  the  disturbance  of  the 
intrathoracic  pressure  still  further  aggravates  the  situation.  Sudden 
collapse  of  an  entire  lung  is  attended  by  all  the  phenomena  of  shock, 
namely,  pallor,  a  clammy  skin,  marked  anxiety  and  a  rapid,  feeble  pulse. 


448         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

In  addition  there  is  air  hunger  and  the  breathing  is  hurried  and  tumultu- 
ous. Death  may  occur  instantly,  within  a  few  hours  or  recovery  from 
the  attack  may  gradually  take  place.  If  the  opposite  lung  is  healthy 
or  but  little  diseased,  it  is  able  to  accommodate  itself  to  the  situation 
and  recovery  usually  occurs.  Fatal  cases  occur,  as  a  rule,  in  tuberculous 
individuals  in  whom  the  opposite  lung  is  also  diseased. 

Collapse  of  the  lung  is  also  brought  about  artificially  by  the  introduc- 
tion of  nitrogen  gas  into  the  pleural  cavity.  Aside  from  some  slight 
difficulty  in  breathing  and  a  sense  of  tightness  in  the  chest  lasting  for  a 
few  hours,  the  compression  rarely  produces  any  disturbance.  Occasion- 
ally death  occurs  suddenly  during  or  just  after  the  injection.  The 
cause  of  the  accident  is  not  known. 

Massive  collapse  of  one  of  the  lower  lobes  due  to  paralysis  of  the 
diaphragm  sometimes  develops  with  such  suddenness  and  intensity  as 
to  suggest  a  pulmonary  embolism.  In  other  instances  the  condition 
gives  rise  to  so  few  symptoms  that  the  presence  may  be  overlooked.  The 
condition  is  as  a  rule  transient  in  character.  The  dyspnea  rarely  lasts 
more  than  24  hours.  In  addition  to  the  dyspnea  there  may  be  a  viscid 
expectoration.  This  is  believed  to  be  due  to  the  contents  of  the  collapsed 
lobe  which  are  pressed  into  the  bronchi  and  coughed  up. 

Physical  Signs. — Because  of  the  diversified  conditions  under  which 
atelectasis  occurs,  a  detailed  description  of  the  physical  signs  is  not 
feasible.  In  some  instances  the  condition  does  not  give  rise  to  distinct- 
ive signs  and  its  existence  must  be  a  matter  of  inference,  as  for  example 
in  broncho-pneumonia.  In  those  cases  in  which  the  entire  lung  is 
partially  or  completely  collapsed  as  the  result  of  mechanical  pressure 
the  physical  signs  are  to  be  attributed  to  the  causative  agent  such  as  a 
pleural  effusion  or  air  in  the  pleural  cavity.  The  physical  signs  obtained 
over  the  lung  after  absorption  or  withdrawal  of  fluid  have  been  dealt 
with  under  the  heading,  "Pleural  Effusion." 

In  prematurely  born  or  asthenic  children  the  intercostal  spaces  and 
the  lateral  and  inframammary  regions  of  the  chest  will  be  seen  to  recede 
during  inspiration.  The  percussion  note  over  the  bases  of  the  lungs  is 
usually  impaired  and  the  respiratory  murmur  everywhere  weak.  Inspira- 
tory recession  of  the  interspaces  and  lower  parts  of  the  chest  may  also 
occur  in  cases  of  collapse  associated  with  broncho-pneumonia  and  in 
cachectic  and  weakened  individuals.  In  the  latter,  fine  crepitant  rales 
may  be  heard  as  the  result  of  an  associated  edema. 

Collapse  of  a  lobe  or  portion  thereof  shows  absence  of  expansion, 
some  retraction  of  the  chest  wall,  dulness  on  percussion  and  absent  or 
faint  bronchial  breath  sounds.  If  edema  is  superadded  to  the  collapse, 
fine  crepitant  rales  are  also  heard.  Pasteur  emphasizes  the  importance 
of  noting  the  position  of  the  apex  beat  of  the  heart  in  cases  of  collapse  of 
one  of  the  lower  lobes.  The  displacement  of  the  apex  beat  is  always 
toward  the  affected  side. 

Diagnosis. — When  the  collapse  occurs  suddenly  and  involves  a  large 
portion  of  one  lung  the  condition  may  be  mistaken  for  croupous  pneu- 
monia. The  absence  of  inflammatory  symptoms  and  low  temperature 
together  with  retraction  of  the  chest  wall  and  displacement  of  the  apex 
beat  of  the  heart  serve  to  distinguish  the  two  conditions.  Collapse  of  a 
large  part  of  a  lung  sometimes  occurs  in  children  from  slight  causes, 
especially  catarrhal  conditions.     Hence  when  the  signs  of  consolidation 


DISEASES    OF   THE    LUNGS  449 

are  found  in  a  young  child,  we  must  always  remember  that  they  are  pos- 
sibly due  to  atelectasis  (Gee). 

Considerable  difficulty  is  experienced  in  distinguishing  between 
collapse  of  a  lower  lobe  and  the  presence  of  fluid  in  the  pleural  cavity 
even  when  fluid  has  previously  been  withdrawn.  In  both  conditions 
there  is  absent  or  distant  breath  sounds,  dulness  on  percussion  and  absent 
expansion.  If  the  case  has  been  followed  from  the  beginning  the  gradual 
return  of  the  breath  sounds  can  be  noted  but  when  seen  for  the  first  time 
it  may  be  necessary  to  introduce  an  exploring  needle  to  settle  the  question. 

Emphysema 

By  pulmonary  emphysema  is  meant  an  abnormal  inflation  and 
dilatation  of  the  air  cells,  which  may  be  temporary,  or  as  is  usually  the 
case,  permanent  in  character.  Five  varieties  are  recognized;  chronic 
hypertrophic;  atrophic  or  senile;  acute  vesicular;  interstitial;  and  com- 
pensatory. 

CHRONIC  HYPERTROPHIC  EMPHYSEMA 

The  term  emphysema,  as  usually  employed,  has  reference  to  the 
chronic  hypertrophic  form  which  in  most  instances  is  a  secondary  process, 
the  result  of  some  preexisting  morbid  process  in  the  lungs  or  bronchi. 

Etiology. — Chronic  emphysema  is  rarely  primary  in  character.  The 
essential  feature  of  the  condition  is  the  loss  of  elasticity  in  the  lungs. 
This  may  be  brought  about  by  any  affection  which  causes  a  forcible  and 
more  or  less  continuous  overdistention  of  the  pulmonary  tissue. 

Strumpell  illustrates  this  very  clearly  by  comparing  the  sound  lung 
with  its  normal  elastic  force,  to  a  new  and  very  tense  rubber  band,  while 
the  emphysematous  lung  may  be  compared  to  an  old  and  lax  band  that 
is  overstretched  and  pulled  out.  This  loss  of  elasticity  with  the  resultant 
inability  of  the  lung  to  contract  is  seen  when  the  thorax  of  an  individual, 
subject  to  the  disease,  is  opened.  Instead  of  collapsing  as  does  the  normal 
lung  under  such  circumstances,  the  emphysematous  lung,  being  in  a 
permanent  state  of  inspiratory  inflation,  remains  distended  even  after 
removal  from  the  chest. 

The  expiratory  theory  of  emphysema  was  first  advanced  by  Men- 
delssohn and  later,  and  independently,  by  Sir  William  Jenner.  The  latter 
expressed  his  views  as  follows:  "The  lung  during  expiration  is  com- 
pressed at  different  parts  with  different  degrees  of  force.  The  parietes 
of  the  thorax,  in  consequence  of  their  anatomical  constitution,  yield  to 
the  same  force  at  different  parts  with  various  degrees  of  facility.  The 
chosen  seats  of  emphysema  are  exactly  those  parts  of  the  lung  which  are 
the  least  compressed  during  expiration,  and  which  are  situated  under 
those  portions  of  the  thoracic  parietes  that  give  way  the  most  readily 
before  pressure." 

More  recently  Adami  and  Nicholls  have  explained  the  expiratory 
theory  as  follows:  Take,  for  instance,  the  simplest  example  a  localized 
emphysema  in  which  the  change  affects  one  small  bronchial  tree  and  the 
associated  air  sacs,  the  rest  of  the  lung  being  in  a  normal  state.  The 
primary  difficulty  is  in  the  bronchus  and  this  may  consist  of  a  narrowing 
of  the  lumen  of  the  bronchus,  whether  congenital  or  induced  by  in- 
flammatory thickening,  or  by  the  presence  of  thick  exudate  within  it. 


450  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

In  such  a  case  the  forcible  nature  of  the  inspiratory  act  draws  air  into 
the  air  sacs  while  the  passive  nature  of  the  expiratory  act  may  prevent 
an  equal  amount  of  air  becoming  expired.  The  result  will  be  that  with 
the  successive  acts  of  inspiration,  the  air  sacs  will  become  more  and  more 
distended,  just  as  occurs  in  bronchial  asthma  as  the  result  of  spasm  of  the 
bronchioles.  If  this  overdistention  of  the  alveolar  wall  be  continued, 
the  result  will  be  malnutrition  due  to  interference  with  the  capillary 
circulation  and  this  in  turn  leads  to  atrophy  and  loss  of  elasticity. 

Ever  since  the  researches  of  Louis  and  James  Jackson,  Jr.,  the  heredi- 
tary element,  as  an  underlying  factor  in  the  causation  of  permanent  dilata- 
tion of  the  air  cells,  has  been  accepted.  The  exact  nature  of  this  inherited 
tissue  defect  has  never  been  satisfactorily  explained.  It  is  assumed, 
however,  that  in  families  subject  to  this  affection  there  is  a  quantitative 
or  a  qualitative  lack  of  pulmonary  elastic  tissue,  and  because  of  this  such 
individuals  become  emphysematous  much  more  readily  than  others. 
Emphysema  developing  before  the  middle  period  of  life,  and  particularly 
when  it  manifests  itself  in  youth,  is  probably  the  result  of  a  congenital 
defect  in  the  elastic  elements  of  the  lung.  It  is  also  to  be  noted  that  such 
individuals  not  infrequently  are  subject  to  hay  fever  and  asthma. 

Whether  we  are  willing  to  accept  the  hereditary  theory  or  not  it  is 
certain  that  the  elastic  tissues  of  the  body  tend  to  lose  their  elasticity  with 
advancing  years.  This  is  true  in  regard  to  the  arteries;  that  the  same 
thing  is  true  in  regard  to  the  lungs  is  evident  from  the  fact  that  marked 
emphysematous  changes  are  far  more  often  encountered  in  those  of  ad- 
vanced years  than  in  younger  individuals.  Furthermore,  the  association 
of  chronic  emphysema  and  arteriosclerosis  is  a  very  frequent  one. 

The  influence  of  occupation  in  the  production  of  emphysema  is  a 
fairly  well  established  fact.  Under  these  circumstances  the  emphysema 
may  be  brought  about  in  several  different  ways.  Thus  it  may  be  pro- 
duced by  one  who  habitually  handles  heavy  weights,  by  reason  of  the 
fact  that  heavy  lifting  is  apt  to  be  attended  by  rapid  and  deep  inspira- 
tions, and  also  by  increased  pressure  during  expiration,  owing  to  the 
closure  of  the  glottis,  which  occurs  in  violent  efforts.  This  forcible 
inflation  and  deflation  of  the  lungs,  if  long  continued,  untimately  wears 
out  the  elastic  tissue.  The  playing  of  wind  instruments,  because  of  the 
prolonged  overdistention  of  the  lungs,  is  said  to  operate  in  much  the  same 
manner.  Although  cited  as  a  frequent  cause  of  chronic  emphysema,  we 
are  of  the  belief  that  the  importance  of  this  particular  vocation  has 
been  over-estimated. 

From  the  standpoint  of  occupation,  any  employment  which  subjects 
the  worker  to  the  constant  inhalation  of  fine  dust  particles  must  be  con- 
sidered as  one  of  the  most  potent  factors  in  the  production  of  emphysema. 
In  such  cases  it  is  almost  invariably  secondary  to  a  chronic  bronchitis. 
"Miner's  asthma,"  while  in  some  instances  tuberculous  in  nature,  is  in 
many  others  a  true  hypertrophic  emphysema  having  its  origin  in  a 
chronic  bronchitis,  which  in  turn  developed  as  the  result  of  the  constant 
inhalation  of  fine  particles  of  coal  dust. 

Because  of  the  nature  of  their  employment,  men  are  more  subject 
to  chronic  emphysema,  than  women.  Extensive  pleuritic  adhesions  by 
impeding  the  movements  of  the  lungs  may  lead  to  diminution  of  the 
elastic  force,  probably  as  the  result  of  increased  expiratory  pressure. 

In  the  majority  of  instances,  however,  we  must  consider  chronic 


DISEASES    OF   THE    LUNGS  451 

bronchitis  as  the  most  frequent  and  the  most  important  exciting  factor. 
The  overdistention  under  these  circumstances  is  brought  about  as  fol- 
lows: With  each  coughing  attack  the  glottis  is  closed  and  the  chest 
walls  are  strongly  compressed  by  the  thoracic  muscles.  Thus  in  the 
expiratory  effort  to  overcome  the  obstruction  above  (the  closed  glott;s) 
the  lung  is  overstretched,  the  overdistention  being  first  manifested  in 
those  parts  least  protected,  namely,  the  apices  and  anterior  margins, 
regions  in  which  the  emphysema  is  always  most  marked.  Heavy  lifting, 
as  we  have  already  pointed  out,  acts  in  much  the  same  manner., 

As  a  further  result  of  this  increased  intrathoracic  pressure,  the 
sternum  is  gradually  pushed  forward,  also  the  cartilages,  the  ribs  eventu- 
ally assuming  a  position  approximating  to  that  seen  at  the  end  of  the 
inspiratory  act.     In  other  words  the  chest  becomes  barrel-shaped. 

Finally,  mention  must  be  made  of  the  most  recent  theory  as  to  the 
causation  of  emphysema,  namely,  premature  ossification  of  the  costal 
cartilages.  This  explanation  has  been  advanced  by  Freund,  who  is  of 
the  belief  that  the  ossification  of  the  costal  cartilages  is  the  cause  of  the 
rigid  dilatation  of  the  chest,  and  the  associated  emphysema  rather  than 
one  of  the  results  of  the  latter. 

Although  calcification  of  the  costal  cartilages  is  commonly  present 
in  cases  of  chronic  emphysema,  the  theory  advanced  by  Freund  has 
received  but  little  recognition. 

Morbid  Anatomy. — Chronic  hypertrophic  emphysema  is  a  bilateral 
affection.  While  both  lungs  are  involved  more  or  less  uniformly,  the 
majority  of  cases  show  more  marked  evidences  of  inflation  at  the  apices, 
the  anterior  borders  and  the  inner  surface  near  the  root  of  the  lung. 
The  chest  of  an  emphysematous  individual  is  barrel-shaped,  all  the 
diameters  being  increased  and  particularly  the  antero-posterior.  The 
costal  cartilages  are  usually  lengthened  and  in  addition  may  be  calcified. 
On  opening  the  chest  the  lungs  are  seen  to  be  greatly  inflated  and  cover 
the  heart.  They  do  not  collapse  but  may  even  project  on  opening  the 
chest.  The  lungs  are  pale,  less  crepitant  than  normally,  are  dry  and  give 
the  sensation  of  handling  a  feather  pillow  (Fig.  290).  Scattered  over  the 
pleural  surface  may  be  seen  small  vesicles  the  size  of  a  pinhead;  in  ad- 
vanced cases  the  vesicles  may  attain  the  size  of  peas,  giving  the  lung  a 
bullous  appearance.  A  spontaneous  pneumothorax  sometimes  results 
from  rupture  of  one  of  these  vesicles.  On  section  the  lung  is  seen  to  be 
dry  and  very  little  blood  escapes.  This  is  due  to  the  fact  that  many  of 
the  capillaries  in  the  alveolar  walls  have  been  destroyed  through  stretch- 
ing. The  bronchi  usually  show  evidences  of  a  chronic  bronchitis  and 
some  thickening  of  the  bronchial  wall;  dilatation  of  the  bronchi  may  be 
present  also. 

Microscopically  the  vesicles  are  seen  to  be  distended  and  the  walls 
thin  and  atrophic.  As  a  result  of  the  distention  of  the  alveolar  walls  the 
capillary  circulation  is  interfered  with.  The  capillary  vessels  may  be 
elongated,  narrowed  or  entirely  obliterated.  The  septa  between  adja- 
cent alveoli  become  wasted  and  thin  and  as  the  disease  progresses  they 
rupture.  In  this  way  two  or  more  alveolar  spaces  may  be  thrown  into 
one.  The  blebs  or  vesicles  seen  beneath  the  pleura  and  along  the  free 
margins  are  formed  in  this  way. 

The  effect  of  a  generalized  chronic  hypertrophic  emphysema  is  to 
alter  the  contour  of  the  chest  and  increase  it  in  size;  to  bring  about  a 


452         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

form  of  dyspnea  characterized  by  difficulty  in  expelling  the  air  from  the 
lung;  to  obstruct  the  passage  of  the  blood  through  the  lungs  with  the 
result  that  hypertrophy,  first  of  the  right  heart  and  later  the  left  heart, 
takes  place  and  eventually  cardiac  failure.  Interference  with  the  pul- 
monary circulation  may  lead  also  to  atheroma  of  the  pulmonary  artery. 
Symptoms. — The  chief  symptoms  of  emphysema  are  dyspnea  and 
cough  and  expectoration,  the  latter  symptoms  being  due  to  frequent 
attacks  of  bronchitis  which  finally  becomes  chronic.     The  dyspnea  is  not 


Fig.   290. — Chronic  emphysema.      Dry  specimen. 

apt  to  be  marked  unless  attacks  of  asthma  are  associated;  in  most 
instances  exertion  causes  more  or  less  shortness  of  breath.  The  cough 
and  expectoration  vary  greatly.  Emphysematous  individuals  may  be 
entirely  free  from  these  symptoms  during  the  summer  months  or  if  they 
spend  the  winters  in  a  warm  climate.  During  the  winter  months  they  are 
especially  liable  to  bronchial  attacks.  The  longer  the  disease  has  lasted 
the  more  likely  is  there  to  be  associated  with  it  a  chronic  bronchitis. 

As  the  individual  advances  in  years  the  circulatory  disturbances 
become  more  and  more  marked.  Shortness  of  breath  increases  on  exer- 
tion, cyanosis  is  often  noted  and  finally  the  picture  is  that  of  failing 
compensation. 


DISEASES    OF    THE    LUNGS 


453 


Physical  Signs. — Inspection. — Emphysema  of  varying  grades  of 
severity  may  be  encountered,  but  the  well-developed  case  presents  certain 
features  which  render  it  easy  of  recognition  almost  at  a  glance.  The 
patient,  while  usually  well  nourished  is  seen  to  be  somewhat  cyanotic, 
sometimes  to  a  very  marked  degree;  the  veins  of  the  neck  are  distended; 
the  sternocleido  muscles  are  conspicuous  and  the  neck  seems  shorter 
than  normal.  The  clavicles  are  prominent  and  the  fossa?  above  them 
unusually  deep.  The  most  characteristic  feature,  however,  is  the  forma- 
tion of  the  chest,  which  is  in  a  permanent  inspiratory  position,  or  as  it 
has  been  aptly  termed,  "barrel-shaped."  The  sternum  projects,  thus 
tending  to  increase  the  antero-posterior  diameter  of  the  chest,  until  it 


Fig.  291. — Chronic  emphysema. 


may  equal  the  length  of  the  lateral  diameter.  The  increase  in  the  antero- 
lateral diameter  is  also  augmented  by  the  exaggeration  of  the  normal 
dorsal  curve  which  gives  the  back  a  bowed  appearance  (Fig.  291).  The 
deepening  of  the  chest  tends  also  to  shorten  it  from  above  downward 
with  the  result  that  the  ribs  are  in  closer  approximation.  The  lower 
ribs  incline  downward  but  slightly  and  may  even  become  straight.  (See 
Figs.  13,  25,  33.) 

The  chest  of  the  typically  emphysematous  patient  has  very  little 
lateral  expansion,  but  moves  up  and  down  as  a  whole,  especially  in  forced 
breathing. 

The  apex  beat  of  the  heart  is  not  visible,  partly  by  reason  of  some 
displacement  downward  and  inward,  and  partly  from  being  covered 
by  the  distended  lung.  For  this  reason  marked  epigastric  pulsation  is 
not  uncommon  in  these  cases. 

Palpation. — Palpation  reveals  little  of  importance.  Vocal  fremitus 
is  normal,  or  at  most  but  slightly  diminished. 

Percussion. — The    percussion    note    obtained    over    emphysematous 


454         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

lungs  is  more  or  less  characteristic  and  has  been  variously  designated  as 
hyperresonant,  vesiculotympanitic  or  "box-like"  in  quality. 

Austin  Flint  taught  that  emphysema  was  always  greater  in  the  left 
upper  lobe  than  elsewhere  and  that  for  this  reason  an  error  was  sometimes 
committed  in  assuming  that  the  less  resonant  note  beneath  the  right 
clavicle  was  due  to  impairment,  when  in  reality  it  was  simply  a  diminu- 
tion in  intensity. 

As  has  been  pointed  out,  the  heart  is  entirely,  or  in  large  part,  covered 
by  lung  tissue.  For  this  reason  the  area  of  cardiac  dulness  is  absent  or 
greatly  reduced  even  when  a  considerable  degree  of  cardiac  hypertrophy 
is  present. 

Owing  to  the  distention  of  the  lungs,  the  area  of  pulmonary  resonance 
is  greatly  increased  downward,  both  anteriorly  and  posteriorly.  The 
upper  border  of  liver  dulness  is  then  lower  than  normal,  and  the  reso- 
nance may  extend,  in  extreme  cases,  as  low  as  the  costal  margin.  With 
failure  of  the  right  side  of  the  heart,  liver  dulness  may  extend  far  below 
the  costal  margin  as  the  result  of  hepatic  engorgement. 

Posteriorly  the  lungs  may  extend  below  the  line  of  the  tenth  rib, 
which  is  the  lower  limit  in  a  normal  chest.  The  percussion  note  at  the 
bases  may  be  impaired  if  there  is  much  secretion  present  in  the  lungs. 

Auscultation. — In  some  instances,  the  only  noticeable  alteration  in 
the  breath  sounds  is  a  slight  diminution  in  the  intensity  of  the  respira- 
tory murmur,  without  other  changes  either  as  to  quality  or  rhythm;  or 
the  respiratory  murmur  may  be  so  feeble  as  to  be  inaudible.  It  is  impor- 
tant to  bear  these  facts  in  mind,  as  the  commonly  accepted  teaching  is 
that  an  alteration  in  the  rhythm  of  the  respiratory  murmur  is  character- 
istic of  the  condition.  The  alteration  in  the  rhythm  consists  in  a  short- 
ening of  the  inspiratory  phase  and  a  lengthening  of  the  expiratory  phase, 
so  that  in  extreme  cases  the  normal  ratio  may  be  reversed — 4  to  1, 
instead  of  1  to  4.  In  some  instances  the  inspiratory  sound  may  be  entirely 
wanting,  the  expiratory  sound  alone  being  heard.  The  expiratory  sound  is 
low  in  pitch  and  non-tubular  in  quality,  thus  differing  from  the  prolonged 
tubular  and  high-pitched  expiratory  sound  heard  over  consolidation. 

Vocal  fremitus  is  normal  or  but  slightly  diminished. 

The  presence  of  rales  is  dependent  on  the  coexistence  of  chronic 
bronchitis  or  asthma  or  both.  If  the  former,  the  rales  are  large  and  small, 
the  latter  being  especially  noticeable  at  the  bases.  If  the  patient  is  in 
addition  asthmatic,  auscultation  will  reveal  from  time  to  time  large 
sonorous  and  piping  sibilant  rales.  These  rales  may  be  so  numerous  as 
to  completely  obscure  the  breath  sounds  and  may  even  be  heard  at  some 
distance  from  the  patient.  The  heart  sounds  are  somewhat  muffled  ow- 
ing to  the  intervening  lung  tissue.  The  second  pulmonic  sound  is  accen- 
tuated as  the  result  of  stasis  in  the  pulmonary  circulation.  In  a  certain 
proportion  of  cases  a  functional  murmur  is  heard  at  the  apex.  With  the 
gradually  increasing  embarrassment  of  the  right  heart  the  cardiac 
phenomena  become  more  and  more  marked,  but  differ  in  no  particular 
from  failing  compensation  due  to  other  causes. 

SENILE  EMPHYSEMA 
(Small  Lunged  Emphysema;   Senile  Atrophy  of  the  Lungs) 

In  the  strict  sense  of  the  word  this  is  not  a  true  emphysema  at  all. 
As  the  name  indicates,  it  is  encountered  in  those  of  advanced  years,  and 


DISEASES    OF   THE    LUNGS  455 

is  but  one  of  the  atrophic  changes,  which  are  commonly  met  with  in  the 
aged. 

Morbid  Anatomy. — When  the  chest  is  opened  the  lungs  readily 
collapse.  They  are  small,  dry,  easily  compressible  and  as  a  rule  deeply 
pigmented.  The  heart  instead  of  being  completely  bidden,  as  in  the  case 
of  hypertrophic  emphysema,  is  more  exposed  than  is  normal.  The 
vesicles  are  usually  enlarged  as  the  result  of  wasting  of  the  septa.  Large 
bullae  are  not  common,  but  are  occasionally  encountered  along  the  free 
margin  of  the  lung.  Owing  to  the  fact  that  a  catarrhal  inflammation  of 
the  bronchial  mucous  membrane  is  almost  always  present,  the  bronchial 
walls  are  thin,  and  at  times  slightly  dilated. 

Symptoms. — There  are  no  symptoms  distinctive  of  senile  emphy- 
sema, but  individuals  so  affected  have  usually  suffered  from  a  winter 
cough  and  shortness  of  breath  for  years.  If  the  bronchi  become  suffi- 
ciently dilated  the  expectoration,  several  times  a  day,  of  large  quantities 
of  sputum  may  occur.  It  is  advisable  to  examine  the  sputum  of  all 
such  patients,  as  a  very  latent  and  chronic  tuberculosis  may  present  exactly 
the  same  picture. 

Physical  Signs. — Inspection. — Individuals  subject  to  this  condition 
are  invariably  of  advanced  years  and  present  a  shrivelled,  withered-up  ap- 
pearance. The  thorax  is  rigid.  The  lower  ribs  are  very  obliquely  placed, 
and  may  be  in  actual  contact.  The  expansion  movements  of  the  chest 
are  much  less  than  normal. 

There  is  no  displacement  of  the  cardiac  impulse. 

Palpation. — Vocal  fremitus  is  normal,  or  at  least  but  little  diminished. 

Percussion. — The  percussion  note  is  hyperresonant  with  an  under- 
lying tympanitic  quality,  partly  the  result  of  the  rigid  chest  wall,  and 
partly  the  result  of  the  large  air  vesicles  and  dilated  bronchi.  The 
superficial  area  of  cardiac  dulness  is  normal,  or  slightly  increased,  be- 
cause of  the  atrophied  lungs. 

Auscultation. — -The  vesicular  murmur  may  be  feeble  and  the  expiration 
prolonged;  on  the  other  hand,  it  may  be  practically  normal.  Rales, 
both  large  and  small,  are  present  especially  in  the  winter  months. 

ACUTE  VESICULAR   EMPHYSEMA 

This  condition  is  a  dilatation  rather  than  an  emphysema  of  the  air 
cells,  there  being  no  structural  change  in  the  alveolar  cells.  It  is  encoun- 
tered in  individuals  who  have  died  from  acute  bronchitis  involving  the 
smaller  tubes,  or  in  asphyxia,  if  accompanied  by  violent  inspiratory 
efforts.  It  is  also  encountered  in  any  condition  which  obstructs  the  air 
from  entering  portions  of  the  lung,  thus  throwing  a  strain  on  the  alveoli 
in  other  parts. 

The  percussion  note  may  be  hyperresonant  and  the  area  of  pulmonary 
resonance  increased.     High-pitched  piping  rales  are  usually  present. 

INTERSTITIAL  EMPHYSEMA 

This  form  is  characterized  by  the  formation  of  large  bullae  in  the 
interlobular  and  subpleural  tissues.  Rupture  of  one  of  these  large  bullae 
near  the  root  of  the  lung  may  lead  to  the  extravasation  of  air  along  the 
trachea,  and  thence  into  the  subcutaneous  tissues  of  the  neck.     Bullae 


456  DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

situated  beneath  the  surface  of  the  pleura  may  rupture  and  thus  produce 
a  pneumothorax.  Aside  from  these  two  facts,  this  condition  has  no 
clinical  interest.  It  cannot  be  recognized  by  physical  signs,  and  during 
life  its  presence  can  only  be  surmised  in  the  event  of  either  of  the  accidents 
mentioned  above. 

COMPENSATORY  EMPHYSEMA 
(Vicarious  or  Complementary  Emphysema;  Hypertrophy  of  the  Lung) 

Compensatory  emphysema  differs  from  the  forms  considered  above  in 
that  it  is  a  physiological  and  not  a  pathological  process.  The  condition 
may  be  localized  in  parts  of  one  or  both  lungs,  or  it  may  involve  one 
entire  lung.  Both  the  localized  and  the  massive  forms  may  be  transient 
or  permanent  in  character. 

Any  acute  inflammatory  affection  of  the  lungs  may  be  accompanied 
by  a  temporary  form  of  emphysema.  It  is  quite  a  common  finding  in 
the  lungs  of  those  who  have  died  from  broncho-pneumonia.  In  such 
cases  the  air  vesicles  between  the  areas  of  consolidation  are  somewhat 
larger  than  normal.     This  form  is  not  recognizable  clinically. 

Localized  emphysema,  compensatory  in  nature,  also  occurs  in  certain 
chronic  affections  of  the  lungs,  notably  in  tuberculosis  of  the  apices, 
during  both  the  active  and  healed  stages  of  that  disease.  This  is  of  con- 
siderable importance  as  the  emphysema  may  mask  the  physical  signs  which 
otherwise  would  be  detected  over  the  infiltrated  area  in  the  incipient  stage 
of  tuberculosis.  It  may  become  permanent  in  character  as  one  of  the 
sequences  of  a  healed  tuberculous  lesion. 

The  massive  form  is  brought  about  by  both  acute  and  chronic  pul- 
monary or  pleural  affections.  In  its  temporary  form  it  is  most  frequently 
seen  in  association  with  a  pleural  effusion,  as  a  result  of  which  the  lung 
on  the  affected  side  is  entirely  or  in  large  part  unable  to  functionate. 
In  the  case  of  a  serous  effusion,  whether  as  the  result  of  an  inflammation 
of  the  pleura  itself,  or  as  a  consequence  of  chronic  cardiac  disease,  the 
vicarious  duty  of  the  opposite  lung  ceases  with  the  withdrawal  or  absorp- 
tion of  the  effusion,  and  the  reexpansion  of  the  compressed  lung.  If, 
however,  the  effusion  is  purulent  in  character,  and  is  not  promptly  drained, 
the  lung  on  the  affected  side  becomes  firmly  and  permanently  anchored 
in  its  compressed  position.  The  compensatory  emphysema  then  becomes 
permanent  and  constitutes  a  true  hypertrophy  of  the  lung.  Extensive 
tuberculous  disease  of  one  lung,  especially  of  the  chronic  type  with  ex- 
tensive fibroid  changes,  also  leads  to  a  marked  degree  of  compensatory 
emphysema  of  the  opposite  side.  And  this  is  true  of  any  chronic  inflam- 
matory disease  affecting  one  lung  alone.  In  other  words  the  presence 
of  a  pathological  lesion  involving  all  or  a  considerable  portion  of  one  lung 
is  practically  always  accompanied  by  a  compensatory  emphysema  of 
the  opposite  side. 

Physical  Signs. — In  some  instances  the  hypertrophy  of  the  unaffected 
lung  is  extraordinarily  great.  This  may  be  apparent  on  inspection  alone. 
The  sound  side  is  seen  to  be  much  larger,  and  the  range  of  the  expansile 
movements  unusually  large.  This  is  more  apparent  because  of  the 
absent  or  very  restricted  motion  of  the  opposite  or  diseased  side.  Further- 
more, the  latter  side  is  not  uncommonly  retracted.  If  the  right  lung 
is  hypertrophied,  the  apex  beat  of  the  heart  will  be  seen  to  have  been 
displaced  to  the  left,  partly  because  of  the  mediastinal^contents  being 


DISEASES    OF    THE    LUNGS 


457 


crowded  over  to  the  left  by  the  enlarged  lung,  and  partly  because  it  is 
pulled  over  by  fibroid  changes  on  the  left  side.  In  some  instances  with 
right-sided  hypertrophy  and  left-sided  disease,  the  heart  is  drawn  up- 
ward, the  apex  beat  being  most  marked  in  the  fourth  or  even  the  third 
interspace.  If  the  left  lung  is  hypertrophied  and  the  right  diseased, 
the  heart  is  displaced  to  the  right  in  exactly  the  same  way.  In  both 
instances  the  extent  of  the  hypertrophy  on  the  one  hand,  and  the  disease 
on  the  other  will  determine  how  great  the  displacement  will  be.  It  is 
not  uncommon  to  see  the  heart  partly  pushed  and  partly  pulled  so  far  to 
the  right  as  to  resemble  a  case  of  dextro-cardia. 

The  displacement   of  the  heart  toward  the  diseased  side  instead  of 
away  from  it,  distinguishes  this  condition  at  once  from  a  pleural  effusion. 


Fig.   292. — Chronic  fibroid  tuberculosis  of  right  lung.      Compensatory  emphysema  of  left 
lung  which  extends  to  the  right  border  of  the  sternum. 


Palpation  confirms  most  of  the  above  findings.  (In  addition  there 
may  be  tactile  changes  over  the  diseased  side;  but  the  changes  are  apt  to 
be  variable,  depending  to  a  great  extent  on  the  degree  of  the  fibroid 
changes  in  the  lung  and  pleura.)  Over  the  hypertrophied  side  the  tactile 
phenomena  are  usually  normal,  or  but  slightly  increased. 

Percussion. — It  should  be  recalled  that  the  anterior  edges  of  the  lungs 
do  not  extend  to  the  middle  line  anteriorly,  and  that  posteriorly  the  bases 
are  on  a  level  with  the  tenth  dorsal  vertebra.  (See  Figs.  67  and  68.) 
With  hypertrophy  of  one  lung  the  anterior  border  will  be  found  beyond 
the  mid-sternal  line,  and  in  extreme  cases  may  extend  ;is  much  as  2  or  3 
inches  into  the  opposite  side  (Fig.  292).  Posteriorly  the  resonance  may 
extend  from  l-i  to  2  inches  below  the  normal  limit.     The  anterior  bolder 


458  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

and  base  of  the  affected  side,  on  the  other  hand,  are  retracted.  In 
tuberculosis  it  sometimes  happens  that  the  hypertrophiecl  or  healthy  lung- 
extends  so  far  into  the  diseased  side  that  it  becomes  infected  by  direct 
contact.  (See  Fig.  183.)  One  instance  is  recalled  in  which  a  cavity 
located  during  life  in  the  left  lung  was  shown  at  the  autopsy  table  to  be 
in  the  anterior  border  of  an  enormously  hypertrophied  right  lung,  which 
extended  far  over  into  the  left  chest. 

Auscultation  shows  no  abnormalities  other  than  the  exaggerated 
character  of  the  vesicular  murmur.  This  is  very  loud  and  is  more  harsh 
than  normal.  It  bears  a  very  strong  resemblance  to  the  puerile  type  of 
breathing  met  with  in  young  children.  The  vocal  resonance  is  normal  or 
but  slightly  increased. 

Pulmonary  Abscess 

Abscess  of  the  lung  is  usually  secondary  to  some  primary  inflamma- 
tion of  the  lung  tissue;  as  the  result  of  extension  from  an  adjoining  organ, 
such  as  cancer  of  the  esophagus  or  abscess  of  the  liver;  and,  finally,  it 
may  be  one  of  the  manifestations  of  a  general  pyemic  process. 

Abscess  of  the  lung  may  be  either  single  or  multiple.  Inasmuch 
as  the  exciting  causes,  the  symptoms  and  the  physical  signs  of  the  two 
forms  of  abscess  present,  as  a  rule,  certain  marked  differences,  they  will 
be  described  separately. 

SINGLE  ABSCESS 

Etiology. — Local  lesions  within  the  chest  play  the  predominant  etio- 
logical role  in  the  case  of  a  single  abscess.  In  a  series  of  30  cases  of  single 
pulmonary  abscess  reported  by  the  authors1  the  exciting  causes  were  as 
follows : 

Croupous  pneumonia 9 

Vegetative  endocarditis  (infarct) .  _ 4 

Suppuration  in  the  abdomen. 4 

Broncho-pneumonia 2 

Rupture  of  cancer  of  esophagus  into  the  lung 1 

Thrombosis  of  branch  of  pulmonary  artery  (typhoid) 1 

General  septicemia 1 

Not  determined 8 

Total 30 

The  importance  of  croupous  pneumonia  is  shown  by  the  fact  that  the 
abscess  followed  that  disease  in  one-third  of  the  cases.  In  nearly  another 
third  of  the  cases  it  was  not  possible  to  determine  the  exciting  cause. 
It  is  quite  possible  that  in  the  case  of  an  apparently  primary  abscess, 
the  original  source  of  the  trouble  was  a  latent  and  unrecognized  pneumonia. 

Within  the  past  few  years  attention  has  been  directed  to  the  frequency 
with  which  a  pulmonary  abscess  follows  operations  on  the  upper  respira- 
tory tract  and  particularly  after  tonsilectomy.  Manges2  and  Claytor3 
have  reported  a  number  of  cases.  The  pulmonary  abscess  may  develop 
either  as  the  result  of  a  septic  embolus,  which  enters  the  circulation  at 
the  seat  of  the  operation,  or  by  direct  inspiration  of  infected  material 

1Noeeis  and  Landis:  Trans.  Assoc.  Am.  Phys.,  1913. 

2  Amer.  Jour,  of  Surgery,  March,  1916. 

3  International  Clinics,  Twenty-sixth  Series,  vol.  ii,  1916. 


DISEASES    OF    THE    LUNGS 


459 


during  the  period  of  anesthesia.  Caseous  foci  in  the  tonsils  seem  to  be 
especially  dangerous  and  for  this  reason  the  tonsils  should  be  removed 
with  as  little  trauma  as  possible. 

A  pulmonary  abscess  may  be  one  of  the  sequels  of  a  traumatic  injury 
to  the  chest,  such  as  violent  contusion  of  the  chest  wall,  a  fractured  rib, 
or  a  penetrating  gunshot  or  stab  wound. 

In  addition  to  the  above-mentioned  causes  of  single  abscess,  I  have 
had  under  observation  two  cases  in  which  the  abscess  was  caused  by  a 
foreign  body — in  one  case  a  tooth  and  in  the  other  a  brass-headed  tack. 
The  importance  of  foreign  bodies  as  an  etiological  factor  of  pulmonary 
abscess  is,  as  the  result  of  X-ray  examinations,  bronchoscopy,  and  of 
increasingly  frequent  operative  intervention  becoming  more  evident. 
In  a  series  of  25  cases  Kltibsl  reports  7  as  being  caused  by  a  foreign  body 
and  Guirez2  has  recorded  5. 


4  cases 


1  case 


4  subdiaphrag- 
matic 


Fig.  293. — Location  of  abscess.     Circles  indicate  site  and  size  of  abscess. 

Morbid  Anatomy. — In  our  series  the  abscess  involved  the  right  lung  in 
19  and  the  left  in  11  cases.  Figs.  293  and  294  show  the  site  of  the  abscess. 
It  will  be  noted  that  21  of  the  30  were  located  in  the  lower  lobes.  This 
is  in  accordance  with  the  findings  of  others.  Walker3  in  132  cases  col- 
lected from  the  literature,  found  the  following  distribution:  upper  lobes 
21;  lower  lobes  76;  middle  lobe  (right  side)  2;  both  upper  and  lower 
lobes  5;  in  28  instances  the  lobe  was  not  indicated.  Not  only  are  the 
lower  lobes  the  points  of  election  but  the  right  side  is  involved  about 
three  times  as  often  as  the  left.  This  is  doubtless  due  to  the  more  fre- 
quent occurrence  of  croupous  pneumonia  in  the  right  lower  lobe.  The 
size  of  the  single  abscess  varies  greatly,  ranging  from  the  size  of  a  small 
marble  to  one  with  a  diameter  of  from  10  to  12  cm.  (Figs.  293  and  294). 

1"Ueber  Lungenabszesse  und  Bronchiektasen,'"  Muteilungen  aus  den  Grenzgebieten 
der  Medizin  u.  Chirurgie,  Heft  3,  549. 

2  Bull,  de  la  Societie  de  Pediatric  de  Paris,  1912,  xiv,  56. 

3  Boston  Med.  &  Surg  Jour.,  July  9,  1914. 


460  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

A  pulmonary  abscess  is  usually  round  in  shape.  The  involved  area 
may  be  gray,  yellow,  reddish,  or  of  a  reddish-yellow  color.  On  section 
it  is  composed  of  thick  yellowish  or  whitish  yellow  or  blood-stained  pus. 
The  pus  may  be  odorless  or  it  may  have  a  sweetish  or  a  very  foul  odor. 
If  the  abscess  is  recent  and  actively  progressing,  the  wall  is  composed  of 
soft  necrotic  lung  tissue.  Immediately  surrounding  this  there  is  an 
area  of  intense  hyperemia  and  edema.  If  the  abscess  is  located  near  the 
surface,  the  overlying  pleura  will  show  some  cloudiness  and  congestion. 

When  the  abscess  has  existed  for  some  time,  connective  tissue  de- 
velops in  the  wall' thus  limiting  and  encapsulating  the  pus.     The  longer 


3  cases 


2  cases 


1  case 


9  cases 


Fig    294. — Location  of  abscess.     Circles  indicate  site  and  size  of  abscess. 


the  abscess  remains  the  thicker  and  more  dense  the  wall  becomes.  Fig. 
295  shows  a  dense  shadow  in  the  right  upper  lobe  due  to  a  large  abscess. 
Fig.  296  shows  the  same  case  after  the  abscess  had  spontaneously  emptied 
itself.  Occasionally  instead  of  a  well-defined  abscess  there  is  an  area  of 
partially  broken-down  lung  tissue  infiltrated  with  pus  and  having  the 
appearance  of  a  sponge. 

A  single  abscess  may  be  acute  or  chronic.  In  the  chronic  type  the 
pus  either  becomes  completely  walled  off  or  is  not  effectively  drained. 
In  either  case  it  acts  as  a  foreign  body  and  the  lung  in  the  vicinity  of  the 
abscess  becomes  fibroid.  Even  a  relatively  small  abscess  may  lead  to 
extensive  fibroid  changes  with  marked  physical  signs  and  symptoms. 

A  single  abscess  may  terminate  in  one  of  three  ways:  (1)  It  most  fre- 
quently ruptures  into  a  bronchus  and  thus  empties  itself.  If  the  drain- 
age is  efficient,  the  process  heals  and  unless  the  cavity  is  very  large,  noth- 
ing but  a  fibrous  scar  remains.  (2)  The  abscess  may  rupture  through  the 
pleura.  If  this  happens  a  pyo-pneumothorax  sometimes  results.  The 
more  usual  course,  however,  is  the  formation  of  an  extrapulmonary 
abscess.     Under  these  circumstances  the  pus  may  become  encysted  in 


DISEASES    OF    THE    LUNGS 


461 


Fig.  295. — Pulmonary  abscess  in  right  upper  lobe.     (Posterior  view.) 


Fig.  296. — Same  after  spontaneous  evacuation.      (Anterior  view.) 


462         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

an  interlobar  fissure,  between  the  base  of  the  lung  and  the  diaphragm  or 
between  the  chest  wall  and  the  lung.  When  an  abscess  forms  near  the 
surface  of  the  lung,  the  pleura  becomes  inflamed  and  the  two  sur- 
faces adhere.  This  acts  as  a  defensive  barrier  if  the  pus  breaks 
through  the  pleura  and  prevents  the  occurrence  of  a  pyo-pneumothorax. 
Robinson  is  of  the  opinion  that  the  majority  of  instances  of  encapsulated 
empyemata  have  their  origin  in  a  pulmonary  abscess  which  ruptures 
through  the  pleura.  (3)  The  abscess  may  become  chronic  and  be  the 
cause  of  extensive  fibroid  changes  in  the  adjacent  lung  tissue. 

Symptoms. — An  abscess  is  to  be  suspected,  if  in  the  presence  of  one 
of  the  known  etiological  factors,  the  patient  develops  respiratory  symp- 
toms or  if  already  present,  these  symptoms  become  aggravated.     In  a 


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Fig.  297. — Pulmonary  abscess. 


typical  case  there  is  an  intermittent  type  of  fever  (Fig.  297),  chills,  some 
sweating  while  the  blood  count  shows  a  high  leukocytosis.  Cough  and 
some  expectoration  are  present  and  chest  pain  is  not  uncommon,  espe- 
cially if  the  pleura  is  involved.  Owing  to  the  fact  that  the  abscess  is  a 
secondary  condition  the  symptoms  indicative  of  its  presence  may  be 
masked  or  misinterpreted  by  reason  of  the  primary  trouble. 

In  the  cases  following  pneumonia,  cough,  expectoration,  fever  and 
pain  in  the  chest  are  already  present.  If  the  fever  persists  and  is  inter- 
mittent with  chills  and  sweats  or  fever  develops  after  a  decline,  a  pul- 
monary abscess  should  be  thought  of.  It  is  to  be  borne  in  mind  that  a  lung 
abscess  is  more  frequently  encountered  in  the  post-mortem  room  than 
at  the  bedside.  In  our  series  the  symptoms  were  either  not  characteristic 
or  entirely  lacking  in  two-thirds  of  the  cases. 


DISEASES    OF    THE    LUNGS  463 

The  diagnosis  is  rarely  made  prior  to  or  in  the  absence  of  the 
sudden  expectoration  of  a  large  quantity  of  purulent  sputum.  This 
constitutes  the  characteristic  feature  of  pulmonary  abscess  and  from  this 
one  symptom  the  diagnosis  can  be  made  with  almost  absolute  certainty. 
The  sputum  is  often  thick  and  ropy  and  pale  yellow,  bloody,  reddish 
brown  or  greenish  in  color.  It  may  be  odorless,  slightly  sweetish  or  very 
foul.  Following  the  initial  outpouring  of  the  pus,  the  process  is  repeated 
at  intervals.  Each  succeeding  time  the  amount  becomes  less  and  less  and 
finally,  in  the  favorable  cases,  ceases  with  the  healing  of  the  pulmonary 
lesion. 

With  the  evacuation  of  the  pus  the  constitutional  symptoms  cease, 
sometimes  at  once.  If  the  drainage  is  inefficient  and  intermittent,  the 
sputum  becomes  fetid  and  the  constitutional  symptoms,  indicative  of 
toxic   absorption,   more  severe. 

The  sputum  is  negative  for  tubercle  bacilli.  The  presence  of  elastic 
tissue  points  very  strongly  toward  the  presence  of  a  pulmonary  abscess. 
Its  absence,  however,  does  not  rule  out  the  presence  of  an  abscess.  By 
pouring  the  sputum  on  a  piece  of  glass  with  a  black  background,  pieces 
of  lung  tissue  may  be  picked  out.  The  elastic  tissue  appears  as  grayish- 
yellow  spots  which  are  selected  for  examination  under  the  microscope. 
If  there  is  no  macroscopic  evidence  of  broken-clown  lung  tissue,  the  spu- 
tum should  be  stained  with  one  of  the  elastic  tissue  stains,  such  as 
Weigert's. 

The  symptoms  of  a  chronic  abscess  are  not  distinctive  and  the  eti- 
ology is  often  obscure.  Among  the  cases  seen  at  the  Phipps  Institute 
suspected  of  having  this  condition  there  was  a  history  of  cough  for  months 
and  the  presence  of  purulent  sputum  which  did  not  contain  tubercle 
bacilli.  The  constitutional  symptoms  were  slight  and  the  general  health 
fairly  good.  They  were  all  referred  to  the  dispensary  as  having  tuber- 
culosis. In  two  an  X-ray  examination  indicated  the  probable  existence 
of  an  abscess. 

Physical  Signs. — The  physical  findings  in  cases  of  abscess  are  not  at 
all  uniform.  In  those  instances  in  which  the  abscess  is  secondary  to 
pulmonary  inflammation  there  are '  already  present  signs  which  may 
mask  its  presence.  In  three  of  the  cases  we  have  reported  a  pleural 
exudate  obscured  the  signs. 

The  only  distinctive  features  are  the  signs  indicative  of  a  cavity, 
i.e.,  tympany  on  percussion,  whispering  pectoriloquy,  amphoric  or  caver- 
nous breathing  and  consonating  rales.  Any  one  or  two  of  these  signs  may 
be  wanting.  Whether  these  signs  can  be  elicited  or  not  will  depend  on 
whether  the  abscess  has  emptied  itself  and  formed  a  cavity  and  also  on 
the  location  of  the  excavation.  If  empty  and  superficially  placed  the 
signs  can  be  obtained  easily.  If  the  cavity  is  deeply  placed  in  the  center 
of  the  lower  lobe,  physical  signs  are  wanting.  As  the  majority  of  single 
abscesses  are  so  situated  it  is  not  surprising  that  the  signs  of  excavation 
are  so  frequently  absent. 

In  8  of  the  30  cases  in  our  series  signs  of  a  cavity  were  present.  The 
area  about  the  angle  of  the  scapula  is  the  most  frequent  site  of  the  cavity 
signs.  When  located  at  the  apex  a  sputum  examination  is  the  only  means 
of  differentiating  the  condition  from  tuberculosis.  In  the  absence  of 
cavity  signs  there  are  present  an  impaired  or  dull  percussion  note,  in- 
creased tactile  fremitus,  distant  bronchial  or  broncho-vesicular  breathing 


464         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

and  fine  crepitating  rales.  The  latter  are  due  to  the  surrounding  area  of 
hyperemia  and  edema. 

The  signs  of  chronic  abscess  are  those  of  some  chronic  inflammatory 
condition  of  the  lung.  In  a  case  with  a  history  of  having  had  a  cough  for 
some  time  and  in  which  there  are  signs  of  pulmonary  damage  a  chronic 
abscess  is  to  be  thought  of.  If  the  base  of  the  lung  is  involved,  tubercu- 
losis is  unlikely  but  in  any  event  the  sputum  should  be  examined  for 
tubercle  bacilli.     An  X-ray  examination  may  be  of  service. 

Abscess  of  the  lung,  when  definitely  recognized,  or  even  when  only 
suspected,  belongs  to  that  border-line  group  of  cases  in  which  the  inter- 
nist and  surgeon  should  be  associated  from  the  beginning.  From  the 
nature  of  the  trouble  it  is  the  internist  who  must  recognize  the  trouble 
as  it  is  he  who  first  sees  such  cases.  There  should  be  no  delay  in  calling 
in  a  surgeon.  When  treated  medically  the  mortality  is  about  50  per  cent, 
while  among  those  treated  surgically  the  mortality  is  about  25  per  cent. 

Diagnosis. — The  two  conditions  with  which  a  single  abscess  is  most 
apt  to  be  confused  are  tuberculosis  and  bronchiectasis.  The  acuteness 
of  the  symptoms  in  abscess  and  the  chronic  nature  of  both  tuberculosis 
and  bronchiectasis  are  important  points.  The  absence  of  tubercle  bacilli, 
especially  in  a  case  in  which  the  symptoms  have  existed  for  some  months, 
should  suggest  the  possibility  of  a  chronic  abscess. 

MULTIPLE  ABSCESSES  OF  THE  LUNG 

Etiology. — In  33  cases  of  multiple  abscess  encountered  among  the 
autopsy  records  of  the  Pennsylvania  Hospital  for  a  period  of  fourteen 
years  the  following  etiological  factors  were  noted: 

Mastoid  disease  and  thrombosis  of  the  lateral  sinus  and  internal 

jugular  vein 1 

Otitis  media • 2 

Otitis  media  and  thrombosis  of  the  lateral  sinus  and  internal  jugular 

vein :•.'■:■  ^ 

Thrombosis  of  the  portal  vein  and  mesenteric  veins  and  appendicitis.  2 

Thrombosis  of  iliac  vein • 1 

Broncho-pneumonia ,. 6 

Croupous  pneumonia 3 

Typhoid  fever  and  broncho-pneumonia 2 

Vegetative  endocarditis  infarct 6 

Abscess  of  kidney 1 

of  lip 1 

of  pharynx 1 

of  seminal  vesicles 1 

of  skin 1 

Gunshot  wound  of  chest 1 

Not  determined 2 

Total 33 

The  exciting  causes,  as  shown  in  the  above  table,  are  seen  to  differ  from 
those  encountered  in  the  case  of  a  single  lesion.  In  multiple-abscess 
formation  supper  ative  foci  of  the  most  diverse  kinds  and  at  distant  parts  of 
the  body  play  an  important  role. 

Another  not  infrequent  cause  of  multiple-abscess  formation  is  the  as- 
piration of  food  or  of  septic  material  from  an  infected  focus  in  another 
area  of  the  lungs. 


DISEASES    OF    THE    LUNGS  465 

Morbid  Anatomy. — One  or  both  lungs  may  be  affected;  the  lower  lobes 
are  more  frequently  affected  than  the  upper.  The  number  of  abscesses 
will  depend  on  the  amount  of  aspirated  material  or  the  number  of  in- 
fected pulmonary  emboli.  The  abscesses  may  be  separated  from  each 
other  by  comparatively  healthy  tissue  or  may  be  confluent.  The  affected 
lung  is  usually  congested  and  edematous  and  on  section  the  abscesses 
are  recognized  as  grayish-yellow,  reddish  areas.  On  cutting  through  one 
of  the  abscesses  the  center  is  apt  to  be  broken  down  and  occasionally 
a  cavity  is  formed. 

When  the  abscesses  are  due  to  metastatic  or  septic  emboli  the  lung  on 
section  shows  the  infected  foci  in  all  stages  from  that  of  purulent  infiltra- 
tion to  the  formation  of  the  abscess  and  excavation.  Occasionally  the 
lung  presents  a  honeycombed  appearance  due  to  the  formation  of  numer- 
ous small  cavities. 

Owing  to  the  wide  extent  of  the  infection  in  the  lungs  and  the  serious 
constitutional  disturbance,  an  individual  suffering  from  multiple  abscess 
formation  rarely  lives  long  enough  to  establish  fibroid  changes  in  the 
walls  of  the  cavity.     The  condition  is  rarely  chronic. 

Symptoms. — A  patient  suffering  from  multiple  pulmonary  abscesses 
usually  presents  the  clinical  picture  of  pyemia.  The  fever  is  irregular  and 
remittent  or  intermittent  in  type,  there  are  chills  and  sweats,  and  every 
evidence  of  a  severe  infection. 

A  marked  leukocytosis  is  usually  present.  The  cough  may  be  severe. 
The  expectoration  is  sometimes  profuse  but  rarely,  if  ever,  occurs  paroxys- 
mally  and  in  the  large  quantities  characteristic  of  a  single  abscess.  The 
sputum  is  purulent  and  not  infrequently  bloody.  Elastic  tissue  may  be 
detected  in  the  sputum. 

The  presence  of  abscess  formation  is  to  be  suspected  in  a  patient  who 
is  suffering  from  some  acute  pyogenic  infection,  such  as  mastoiditis  or  acute 
otitis  media,  and  who  in  addition  develops  pulmonary  symptoms.  The 
latter  are  not  always  present  or,  if  so,  may  be  so  mild  as  not  to  attract 
much  attention. 

Physical  Signs. — The  physical  findings  are  even  more  uncertain  in 
multiple  abscess  than  in  the  case  of  'the  single  isolated  lesion.  In  our 
series  of  33  cases  the  following  physical  signs  were  noted: 

Scattered  rales 2 

Scattered  rales  and  friction  rub 4 

Scattered  rales  and  areas  of  dulness 5 

Areas  of  dulness * 

Dulness  at  one  base  alone 6 

Signs  of  cavity 1 

No  record 1 1 

The  signs  enumerated  above  may  be  elicited  in  a  variety  of  pulmonary 
conditions.  They  are  suggestive  of  abscess  formation  only  when  there 
is  a  known  focus  of  suppuration ;  when  there  are  symptoms  indicative  of 
a  general  septic  infection;  and  when,  in  addition,  the  sputum  is  purulent 
or  bloody  in  character  and  occurs  in  fairly  large  amounts. 

Diagnosis. — The  recognition  of  the  presence  of  multiple  abscesses  is 
far  from  easy  and  their  presence  is  unsuspected  even  oftener  than  in  the 
case  of  a  single  abscess.  In  some  instances  their  existence  can  be  sur- 
mised in  cases  of  general  septicemia  which  develop  respiratory  symp- 
toms or  in  cases  of  croupous  or  broncho-pneumonia  in  which  a  hectic  type 

30 


466  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

of  temperature  and  chills  and  sweats  succeed  the  initial  trouble. 
When  there  are  a  number  of  abscesses  involving  both  lungs  or  a  consid- 
erable portion  of  one  lung  and  there  are  no  localizing  signs  the  following 
conditions  must  be  considered — tuberculosis  or  one  of  the  mycotic  in- 
fections. The  examination  of  the  sputum  will  rule  out  or  establish  the 
diagnosis  if  due  to  one  of  these  affections.  If  any  of  the  abscesses  break 
down,  elastic  tissue  also  may  be  present  in  the  sputum. 

PULMONARY    GANGRENE 

For  the  first  accurate  account  of  pulmonary  gangrene  we  are  indebted 
to  Laennec  who  described  two  forms:  the  circumscribed  and  the  diffuse 
(uncircumscribed).  His  description  of  the  morbid  anatomy  and  the 
symptomatology  is  unrivaled  to  the  present  day. 

Etiology. — Gangrene  of  the  lung  is  one  of  the  rarest  of  pulmonary 
affections.  Fowler  in  1621  consecutive  autopsies  encountered  but  7 
examples  of  the  disease  (0.43  per  cent.).  Among  662  autopsies  at  the 
Phipps  Institute  2  instances  of  pulmonary  gangrene  have  been  noted; 
one,  of  the  diffuse  form  in  a  non-tuberculous  subject  and  in  the  other 
the  gangrene  complicated  a  tuberculous  process  (0.30  per  cent.). 

Gangrene  of  the  lungs  is  never  a  primary  condition  but  occurs  second- 
arily in  a  variety  of  conditions.  When  one  comes  to  analyze  the  exciting 
causes  of  pulmonary  gangrene,  it  is  evident  that  there  must  be  other  factors 
at  work  besides  necrosis  of  tissue  and  the  action  of  saprophytic  organisms, 
otherwise  the  condition  would  be  relatively  common.  As  a  rule  gangrene 
is  encountered  in  individuals  whose  resistance  has  been  lowered.  This 
may  be  due  to  a  chronic  debilitating  illness  such  as  diabetes;  to  the  ex- 
haustion incident  to  certain  of  the  insane  states  (dementia,  melancholia) 
and  lastly  to  a  lowering  of  vitality  as  the  result  of  excesses. 

The  following  etiological  factors  have  been  noted : 

1.  It  may  be  the  terminal  event  in  bronchiectasis  and  putrid  bron- 
chitis. In  both  these  conditions  patches  of  septic  broncho-pneumonia 
frequently  develop  and  these  may  become  gangrenous. 

It  has  long  been  recognized  that  gangrene  of  the  lungs  not  infrequently 
occurs  among  the  insane.  In  these  cases  the  exciting  cause  is  an  "  aspira- 
tion" broncho-pneumonia.  In  the  same  manner  a  septic  broncho- 
pneumonia followed  by  gangrene,  may  occur  secondarily  to  cancer  of  the 
mouth,  tongue,  pharynx  or  the  esophagus.  In  rare  instances  gangrene 
of  the  lungs  is  one  of  the  sequels  of  a  broncho-pneumonia  complicating 
measles. 

As  a  sequel  to  croupous  pneumonia  gangrene  is  very  infrequent  and 
when  it  does  occur  it  is  usually  in  a  debilitated  or  diabetic  subject  (Osier). 
As  a  complication  of  pulmonary  tuberculosis  gangrene  is  rare.  Only  one 
instance  has  been  encountered  at  the  Phipps  Institute  among  662 
autopsies.  In  two  other  cases  the  horrible  fetor  of  the  sputum  lead  to 
a  diagnosis  of  gangrene  but  in  neither  case  was  it  found  at  the  autopsy. 
In  one  the  fetor  was  due  to  an  associated  bronchiectasis;  the  other  to 
an  empyema  which  had  ruptured  into  the  lung  and  was  discharging 
through  a  bronchus. 

2.  The  pressure  of  a  mediastinal  tumor  or  aneurism  may  cause 
gangrene.  Such  instances  are  rare,  however.  I  recall  one  case  in  the 
service  of  the  late  Frederick  A.  Packard,  at  the  Philadelphia  General 


DISEASES    OF    THE    LUNGS  467 

Hospital,  in  which  the  pressure  of  an  aneurism  of  the  descending  aorta 
had  severed  completely  the  left  bronchus.  The  distal  portions  of  the 
bronchus  and  the  adjacent  lung  tissue  had  become  gangrenous. 

3.  Gangrene  may  develop  as  the  result  of  an  embolus  lodging  in  a 
branch  of  the  pulmonary  artery.  This  sometimes  occurs  during  con- 
valescence from  an  attack  of  protracted  fever,  such  as  typhoid. 

One  of  the  main  branches  of  the  pulmonary  artery  may  become  throm- 
bosed in  which  case  the  diffuse  type  of  gangrene  is  produced.  It  may 
involve  the  greater  part  of  one  lobe. 

4.  Gangrene  may  be  a  sequel  to  some  traumatic  injury  of  the  lungs. 
From  the  above-etiological  factors  it  will  be  seen  that  gangrene  arises 

under  much  the  same  circumstances  as  abscess  of  the  lung.  In  certain 
instances  an  abscess  may  later  become  gangrenous.  It  seems  highly 
probable  that  the  general  resistance  is  a  strong  deciding  factor.  The 
more  debilitated  the  patient  the  greater  the  likelihood  of  gangrene 
developing. 

Morbid  Anatomy. — Circumscribed  Form. — The  gangrenous  focus  may 
be  single  or  there  may  be  two  or  more.  As  in  the  case  of  abscess,  the 
lower  lobe  is  more  frequently  the  site  of  the  trouble  than  the  upper. 
Walker1  in  an  analysis  of  40  cases  found  the  right  lung  involved  in  21; 
the  left  in  9;  both  sides  in  2;  and  side  not  mentioned  in  8.  The  gan- 
grenous area  is  more  apt  to  be  located  near  the  periphery  of  the  lung  than 
in  the  central  portion. 

Three  stages  are  to  be  recognized :  (1)  The  affected  area  is  moist  but 
firmer  than  the  normal  lung  and  usually  greenish-black  in  color,  though 
it  may  be  of  a  dirty  gray  color.  (2)  The  stage  of  liquefaction  in  which 
the  affected  area  is  converted  into  a  fetid  pulp.  (3)  The  stage  of  excava- 
tion. The  part  of  the  lung  immediately  surrounding  the  gangrenous 
focus  is  deeply  engorged  and  presents  the  appearance  of  hepatization; 
outside  of  this  zone  there  is  marked  edema  of  the  pulmonary  tissue. 

Laennec  described  the  evolution  of  the  process  as  follows:  The 
affected  area  sometimes  detaches  itself  from  the  surrounding  parts  form- 
ing a  slough  of  a  blackish,  greenish,  brownish  or  yellow  color.  This 
slough  may  remain  isolated  in  the  midst  of  the  excavation  formed  by 
the  destruction  of  the  mortified  part.  It  is  more  usual,  however,  for 
the  eschar  to  be  entirely  softened  without  forming  a  separate  slough, 
and  to  be  transformed  into  a  species  of  putrid  pulp,  of  a  dirty  greenish- 
gray,  sometimes  bloody  color,  and  of  a  horrible  fetor.  This  softened  mass 
soon  makes  its  way  through  some  neighboring  bronchus  and  being,  by 
degrees,  evacuated  forms  a  cavity. 

With  the  separation  of  the  eschar  a  cavity  is  formed  with  ragged  and 
shreddy  walls  (Fig.  .298)  which  are  lined  with  a  false  membrane,  of  a 
grayish,  or  dirty  yellow  color  and  which  secretes  a  dirty  turbid  pus  or 
"  black  sanies."  The  lining  membrane  is  soft  and  readily  scraped  off 
with  a  scalpel.  If  the  cavity  is  small  the  false  membrane  may  fill  the 
space  and  be  transformed  into  a  cicatrix.  The  false  membrane  may  be 
wanting.  The  wall  is  then  composed  of  an  infiltrated  zone  which  secretes 
a  foul  pus. 

In  some  instances  blood-vessels  entirely  denuded  and  isolated,  but 
perfectly  intact,  traverse  the  cavity.     In  other  instances  they  are  de- 

1  Boston  Med.  &  Surg.  Jour.,  July  9,   1914. 


468         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

stroyed,  the  open  ends  being  plugged  with  a  thrombus.     Occasionally 
a  fatal  hemorrhage  results  from  the  erosion  of  one  of  these  vessels. 

An  associated  bronchitis  is  nearly  always  present.  Perforation  of 
the  visceral  layer  of  the  pleura  may  produce  a  pyo-pneumothorax. 
Occasionally  a  pleural  effusion  is  noted.  A  hemorrhagic  effusion  occurred 
in  one  case  at  the  Phipps  Institute.  In  rare  instances  the  gangrenous 
eschar  becomes  cicatrized  and  the  patient  recovers. 


Fig.  298. — Gangrene  of  the  lung.     {Philadelphia  Hospital.) 

Diffuse  Gangrene. — This  form  is  very  rare.  It  is  characterized  by 
the  absence  of  a  limiting  zone  of  inflammation  the  gangrenous  area  merg- 
ing into  the  surrounding  lung  tissue.  Not  uncommonly  it  involves  a 
large  part  of  or  even  an  entire  lobe. 

In  a  case  observed  at  the  Phipps  Institute  the  gangrene  resulted  from 
thrombosis  of  the  branch  of  the  pulmonary  artery  leading  to  the  right 
lower  lobe.  The  affected  lobe  was  dark  red  and  very  soft  and  friable, 
but  necrosis  and  breaking  down  of  the  tissue  had  not  occurred.  There 
were  a  number  of  areas  in  which  the  visceral  pleura  had  disappeared. 
In  one  place  there  was  an  infarct  which  was  firmer  and  not  so  dark  in 


DISEASES    OF    THE    LUNGS  469 

color  as  the  surrounding  tissue.  The  denudation  of  the  visceral  pleura 
had  resulted  in  a  pneumothorax  with  a  hemorrhagic  effusion.  The 
patient  had  a  hypertrophied  and  dilated  heart. 

The  bacteriology  of  gangrene  is  varied.  In  addition  to  the  pus- 
producing  germs  there  are  also  numerous  saprophytic  organisms.  It  is 
not  clear  whether  gangrene  can  be  produced  by  the  saprophytes  alone  or 
whether  an  antecedent  infection  with  the  pus-producing  organisms  is 
also  necessary.  It  is  to  be  borne  in  mind  that  a  number  of  cases  of 
gangrene  have  been  reported  in  which  acid-fast  bacilli  have  been  found 
in  the  pus.  Ophuls  places  these  acid-fast  organisms  among  the 
streptotricheae. 

Symptoms. — The  symptoms  of  pulmonary  gangrene  may  occur  un- 
heralded by  any  previous  pulmonary  trouble.  As  a  rule,  however,  this 
is  not  the  case  and  symptoms  of  a  preexisting  pulmonary  lesion  are 
present.  The  premonitory  symptoms  vary  greatly,  depending,  as  they 
do,  on  such  a  variety  of  conditions. 

The  sputum  constitutes  the  characteristic  feature  of  pulmonary  gan- 
grene. It  is  of  a  horribly  fetid  odor  which  may  permeate  the  entire 
house.  If  allowed  to  stand  in  a  conical  glass  it  separates  into  three 
layers:  (a)  a  greenish-brown  heavy  sediment,  (b)  a  middle  layer  of  thin 
greenish  or  brownish  fluid,  and  (c)  a  thick  frothy  top  layer.  The  sputum 
invariably  contains  elastic  tissue,  and  in  some  instances  large  fragments 
of  lung  tissue  have  been  coughed  up.  While  some  observers  claim  that 
elastic  tissue  may  be  absent  Osier  states  that  he  has  never  met  with  such 
an  instance. 

Cough  is  usually  present  and  often  paroxysmal  in  character.  A  frank 
hemoptysis  is  not  unusual  and  may  be  the  first  sign.  Pleuritic  pain  is 
very  common.  While  the  constitutional  symptoms  are  usually  severe, 
they  are  not  distinctive  of  pulmonary  gangrene.  The  temperature  is 
irregular  and  of  the  hectic  type;  the  pulse  is  rapid;  and  the  prostration 
extreme.  There  is  also  a  loss  in  weight  although  death  usually  occurs 
before  the  emaciation  has  progressed  far.  Death,  generally  ensues  as 
the  result  of  exhaustion;  rarely  a  large  hemorrhage  is  the  terminal  event.. 

If  the  gangrenous  area  remains  closed  and  does  not  communicate 
with  a  bronchus  the  fetid  sputum  so  characteristic  of  the  disease  will  be 
absent.  This  so-called  latent  form  is  occasionally  met  with  in  the  post- 
mortem room  in  young  children,  in  the  insane  and  in  diabetic  subjects. 

Physical  Signs. — The  physical  signs  are  not  distinctive.  In  the 
absence  of  the  characteristic  sputa  they  furnish  no  information  as  to  the 
true  nature  of  the  trouble.  In  the  first  stage  before  breaking  down  of 
the  pulmonary  tissue  has  occurred,  there  is  dulness  or  impairment  of 
the  percussion  note  over  the  affected  area.  Later,  when  excavation 
has  occurred,  the  note  may  be  tympanitic. 

The  breath  sounds  may  be  bronchial  or  very  distant  in  character 
during  the  stage  of  engorgement.  Fine  moist  rales  are  present.  Later  in 
the  disease  rales  are  heard  over  both  lungs  as  the  result  of  an  associated 
bronchitis.  Owing  to  the  proximity  of  the  affected  area  to  the  surface 
of  the  lung  a  friction  rub  is  common.  When  the  gangrenous  eschar  has 
been  removed,  signs  of  a  cavity  may  be  heard. 

Diagnosis. — The  characteristic  feature  of  pulmonary  gangrene  is  the 
indescribable  fetor  of  the  sputum.  While  some  claim  that  the  gangren- 
ous   odor    is    distinctive  it   often   cannot   be   differentiated   from  that 


470         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

occurring  in  bronchiectasis,  from  that  coming  from  an  encysted  empyema 
which  ruptures  into  the  lung,  or  a  pulmonary  abscess. 

In  bronchiectasis  there  is  an  absence  of  elastic  tissue.  In  the  case  of 
an  encysted  empyema  or  abscess  the  clinical  distinction  is  not  always 
easily  made.  The  sputum  may  be  horribly  fetid  in  all  three  conditions. 
Elastic  tissue  occurs  in  both  abscess  and  gangrene  and  may  also  be  noted 
in  instances  in  which  the  pus  ruptures  into  the  lung.  Even  at  the  au- 
topsy table  the  distinction  between  a  pulmonary  abscess  and  a  gangrenous 
process  is  sometimes  fraught  with  difficulty. 

PULMONARY  INFARCTION 
(Pulmonary  Embolism — Pulmonary  Apoplexy) 

Etiology. — In  the  recognition  of  this  accident  a  knowledge  of  the 
etiological  factors  which  predispose  to  it  is  of  the  utmost  importance, 
as  without  such  knowledge  the  phenomena,  which  attend  the  lodging  of 
an  embolus  in  a  branch  of  the  pulmonary  artery,  are  apt  to  be  incorrectly 
interpreted. 

The  source,  from  which  pulmonary  emboli  come,  are  to  be  found  either 
in  the  right  side  of  the  heart,  or  in  the  veins  of  the  body.  The  reason  for 
this  is  obvious.  In  order  to  reach  the  pulmonary  circulation  the  embolus 
must,  of  necessity,  pass  directly  from  the  right  ventricle  or  from  smaller 
to  larger  vessels  in  its  course  toward  the  heart,  otherwise  it  would  lodge 
at  some  distal  po;nt.  On  the  other  hand,  an  embolus  finding  lodgment 
in  the  other  viscera  such  as  the  kidney,  spleen,  etc.,  travels  in  the  opposite 
direction,  and  by  way  of  the  arterial  system,  its  source  being  in  the  left 
side  of  the  heart  (simple  or  malignant  endocarditis).  A  pulmonary  em- 
bolism arises  then  under  the  following  conditions: 

1 .  Valvular  Heart  Disease. — Of  the  valvular  lesions  mitral  disease  is  the 
most  important,  particularly  mitral  stenosis.  Aortic  lesions  are  rarely 
associated  with  pulmonary  infarction.  Pulmonary  infarction  due  to 
cardiac  lesions  in  the  left  heart  is  usually  the  result  of  stasis  which  leads 
to  the  formation  of  clots  in  the  pulmonary  artery. 

When  the  embolus  originates  in  the  right  heart  the  process  is  as  fol- 
lows: Fibrin  is  deposited  on  the  auricular  or  ventricular  walls  and  this, 
in  addition  to  slowing  of  the  circulation,  leads  to  coagula  forming  in  the 
interstices  of  the  muscular  bundles.  Eventually  fragments  are  broken 
off  and  escape  into  the  pulmonary  circulation. 

2.  Phlebitis. — The  occurrence  of  a  thrombus  in  some  portion  of  the 
venous  system  is  the  most  prolific  source  of  hemorrhagic  infarction  of  the 
lung.  Venous  thrombi  occur  not  infrequently  in  the  acute  infections, 
especially  typhoid  fever.  Of  the  veins  involved  those  of  the  -lower 
extremities,  especially  the  femoral,  are  perhaps  most  frequently  affected. 
A  venous  embolus  may  consist  of  a  large  fragment  from  a  thrombus  in 
one  of  the  large  veins,  such  as  the  iliac  or  femoral.  Owing  to  its  size  it 
produces  an  infarct  of  large  size  and  if  death  does  not  ensue  immediately, 
the  physical  signs  resemble  those  obtained  in  cases  of  croupous  pneu- 
monia. Large  venous  emboli  are  not  common.  On  the  other  hand, 
small  venous  emboli  are  not  of  infrequent  occurrence.  They  result  from 
the  separation  of  small  fragments  during  the  formation  of  the  thrombus 
and  may  manifest  themselves  by  pulmonary  symptoms  days  before  the 
presence  of  the  thrombus  is  known  to  exist.     Probably  the  best  known 


DISEASES    OF    THE    LUNGS  471 

form  of  venous  thrombosis  is  that  occurring  in  the  puerperal  period,  and 
commonly  referred  to  as  phlegmasia  alba  dolens  or  milk  leg.  In  addition 
it  must  be  borne  in  mind  that  pulmonary  emboli  not  infrequently  come 
from  a  thrombus  formation  in  one  of  the  uterine  veins  following  confine- 
ment. This  usually  occurs  in  the  first  three  weeks  of  the  puerperal 
period;  beyond  the  fifth  week  its  occurrence  is  exceptional. 

Of  recent  years  it  has  come  to  be  a  well-recognized  fact  that  a  pul- 
monary embolism  may  follow  various  operations,  particularly  those  on 
the  abdominal  or  pelvic  organs.  It  is  more  than  probable  that  not  a  few 
cases  of  pneumonia,  following  major  operations,  are  in  reality  instances  of 
pulmonary  infarction.  Venous  thrombosis  may  occur  in  chlorotic  girls, 
in  those  who  are  gouty,  as  a  complication  of  varicose  veins  and  in  those 
who  are  apparently  healthy.  Conner1  has  reported  six  cases  of  pul- 
monary infarction  due  to  venous  thrombosis,  occurring  in  apparently 
healthy  individuals. 

3.  Infected  Emboli. — The  most  serious  form  of  pulmonary  embolism 
is  that  in  which  the  thrombus  harbors  some  microorganism.  In  these 
cases  there  is  added  to  the  danger  of  the  infarct  the  certainty  that  it  will 
develop  into  an  abscess.  Multiple  abscesses  of  the  lung,  having  their 
origin  from  an  infarct,  are  almost  constantly  associated  with  general 
pyemia  or  right-sidecl  malignant  endocarditis. 

4.  Fat  Emboli. — Although  not  of  venous  origin,  a  pulmonary  infarct 
may  be  produced  by  a  fat  embolus  following  fracture  of  one  of  the  bones. 
As  a  rule  the  fat  globules  lodge  in  the  finer  capillaries,  and  rarely  ob- 
struct a  branch  of  the  pulmonary  artery,  sufficiently  large  to  produce 
symptoms.  Bissel  has  reported,  from  the  Mayo  Clinic,  the  finding  of 
fat  emboli  in  the  lungs  following  operations.  The  emboli  may  be  very 
small.  They  are  associated  with  broncho-pneumonic  areas  but  it  is  un- 
certain whether  they  cause  the  pneumonia  or  not.  Cyanosis  is  the  most 
constant  symptom  of  the  condition. 

5.  Foreign  Material. — In  all  forms  of  hypodermic  medication  it  is 
usual  to  emphasize  the  importance  of  being  sure  the  needle  is  not  in  a 
vein,  otherwise  the  injected  material -might  be  carried  directly  into  the 
pulmonary  artery,  and  be  followed  with  serious  results.  An  instance  of 
this  has  recently  come  to  my  notice.  Almost  immediately  following 
an  injection  of  gray  oil  into  the  buttock,  the  patient  presented  all  the 
classical  phenomena  of  pulmonary  embolism,  and  although  he  recovered, 
his  life  was  despaired  of  for  some  hours. 

6.  Air  Emboli. — 'Lastly  we  have  to  consider  the  occurrence  of  air 
emboli.  For  years  the  possibility  of  this  accident  has  been  repeatedly 
emphasized  in  carrying  out  procedures  which  involve  injecting  any  sub- 
stance into  the  veins.  As  a  matter  of  fact,  however,  the  occurrence  of 
such  an  accident  has  never  been  proven,  and  there  are  those  who  disbelieve 
entirely  in  there  being  any  likelihood  of  such  an  accident. 

Morbid  Anatomy. — When  an  embolus  is  detached  from  the  parent 
thrombus  it  is  at  once  swept  along  the  venous  blood  current.  As  it 
passes  through  vessels  which  are  constantly  increasing  in  size,  no  obstruc- 
tion is  offered  in  its  journey  toward  the  right  side  of  the  heart.  On 
leaving  the  right  heart,  the  embolus  enters  the  pulmonary  artery,  and 
here  the  conditions  are  reversed,  as  the  branches  of  the  pulmonary  artery 
are  terminal  vessels.  Depending  on  the  size  of  the  embolus  a  vessel  is 
1  Arch.  Int.  Med.,  March.  1914. 


472         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEUEA,    AND    DIAPHRAGM 

sooner  or  later  reached,  which  is  too  small  to  admit  of  its  further  passage. 
The  block  usually  occurs  at  a  point  where  the  artery  bifurcates.  ^ With 
the  plugging  of  the  vessel  the  pressure  in  the  area  situated  peripherally 
to  the  blocked  point  almost  disappears.  This  results  in  a  backward 
flow  of  blood,  which  stagnates  in  the  affected  area,  and  in  addition  the 
various  elements  of  the  blood  leak  through  the  walls  of  the  vessel,  thus 
saturating  the  tissues  in  the  area  supplied  by  the  plugged  vessel.  The 
area  so  affected  constitutes  the  so-called  hemorrhagic  infarct.  If  there 
has  been  a  preexisting  stasis  in  the  pulmonary  vessels,  such  as  is  met  with 
in  chronic  cardiac  disease,  the  hemorrhagic  character  of  the  infarction 
becomes  more  marked. 


Fig.  299. — Multiple  infarction  of  the  lung. 

Pulmonary  infarcts  are  more  commonly  met  with  in  the  lower,  than 
the  upper  lobes  of  the  lung.  They  are  conical  or  wedge-shaped,  the  base 
being  formed  by  the  visceral  pleura.  The  affected  area  generally  pro- 
jects slightlv  above  the  surface,  the  visceral  pleura  being  covered  with  a 
fibrinous  deposit,  which  may  be  limited  to  the  area  involved,  or  extend 
some  distance  about  it.     The  extent  of  the  infarct  depends  on  the  size 


DISEASES    OF    THE    LUNGS 


473 


of  the  vessel  which  has  been  occluded;  it  may  correspond  to  the  area  of 
one  or  two  lobules  (Fig.  299),  or  may  involve  nearly  an  entire  lobe. 

On  section,  the  wedge-shaped  infarct  is  readily  distinguished  by  the 
black-red  color,  and  the  fragile  condition  of  the  blood-soaked  tissue. 
Pulmonary  infarcts  may  be  entirely  absorbed,  but  as  a  rule  resolution  is 
not  complete  and  a  scar  results.  If  the  infarct  is  of  septic  origin  as  in 
cases  of  right-sided  malignant  endocarditis  or  general  pyemia,  abscess 
formation  results. 

Symptoms. — The  severity  of  the  symptoms,  following  the  lodgment 
of  an  embolus  in  the  lung,  depends  on  the  size  of  the  vessel  blocked. 


Fig. 


300. — Pulmonary  embolism  in  a  patient  convalescing  from  typhoid  fever. 
(Interval  of  one  day  before  the  rise  of  temperature.) 


If  the  embolus  is  a  large  one,  the  patient  may  be  so  severely  shocked  that 
death  occurs  immediately  or  within  an  hour  or  two.  On  the  other  hand, 
the  embolus  may  be  so  small  that  it  produces  no  symptoms  at  all.  When 
a  moderately  large  branch  of  the  pulmonary  artery  is  suddenly  occluded, 
the  patient  is  seized  with  sudden  dyspnea,  cyanosis  and  intense  pain  in 
the  side.  This  is  followed  a  few  hours  later  by  the  expectoration  of  liquid 
or  dark  red  clotted  blood,  which  is  not  frothy,  as  in  the  hemoptysis  of 
phthisis.  An  initial  chill  is  rarely  observed.  Strumpel  states  that  fever 
is  apt  to  be  delayed  a  day  or  so  following  the  formation  of  the  infarct 
(Fig.  300),  and  that  this  is  sometimes  of  service  in  distinguishing  the 
condition  from  lobar  pneumonia. 


474  DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

In  those  patients  in  whom  the  symptoms  are  overwhelmingly  severe, 
the  source  of  the  embolism  is  apt  to  be  in  the  veins,  while  the  less  severe 
instances  are  met  with  in  cases  of  chronic  cardiac  disease. 

Physical  Signs. — The  recognition  of  a  pulmonary  infarction  depends, 
primarily,  on  a  knowledge  of  the  etiological  factor,  and  secondarily,  on 
the  symptoms.  Physical  signs  at  best  will  indicate  only  the  size  of  the 
involved  area.  If,  however,  the  infarction  is  small  or  centrally  located, 
chest  signs  will  be  entirely  wanting. 

Inspection. — So  far  as  the  chest  is  concerned,  inspection  will  be  nega- 
tive unless  a  large  portion  of  a  lobe  is  involved.  If  that  occurs,  expansion 
of  the  affected  side  will  be  diminished. 

Palpation. — Palpation  will  reveal  deficiencies  in  expansion,  if  any 
such  exist.  Vocal  fremitus  will  be  increased  providing  the  infarct  is 
sufficiently  large,  otherwise  no  change  is  apt  to  be  detected. 

Percussion. — Impairment  or  absence  of  pulmonary  resonance  will 
also  depend  on  the  size  of  the  infarct,  and  whether  it  is  peripherally 
located.  The  area  of  dulness  does  not  extend  as  in  pneumonia  and  if 
small  and  circumscribed  usually  disappears  in  two  or  three  days.  If  the 
infarct  is  large,  the  percussion  note  may  be  flat  and  suggest  the  presence 
of  an  effusion.  Dulness  may  change  later  to  tympany  if  the  infarct  breaks 
down  and  an  abscess  results. 

Auscultation. — In  cardiac  cases  rales,  both  large  and  moderate-sized, 
are  apt  to  be  present  throughout  both  lungs  as  the  result  of  stasis.  Local- 
izing signs,  such  as  fine  crackling  rales,  or  a  friction  rub,  are  not  likely 
to  be  present  for  some  time  after  the  formation  of  the  infarct  and  may 
be  the  only  signs  present.  The  breath  sounds,  however,  are  apt  to  be 
absent  or  very  distant  from  the  beginning.  Later,  if  the  effused  blood 
is  absorbed,  the  breath  sounds  return,  and  the  rales  become  coarser  over 
the  involved  area.  In  septic  cases  the  infarct  may  change  into  an  abscess 
and  empty  into  a  bronchus,  thus  forming  a  cavity.  Under  these  circum- 
stances the  signs  over  the  affected  area  differ  in  no  particular  from  cavity 
formation  due  to  other  causes. 

Diagnosis. — Cases  in  which  there  is  an  evident  cardiac  lesion  or  the 
presence  of  a  phlebitis  offer  little  difficulty  in  diagnosis.  In  those  cases 
in  which  the  phlebitis  is  latent  or  is  located  in  veins  inaccessible  to  sight 
or  touch,  the  source  of  the  respiratory  symptoms  may  be  difficult  to 
interpret.  The  sudden  appearance  of  symptoms  and  signs  due  to  a 
pulmonary  infarction  may  be  the  first  intimation  we  have  of  a  venous 
thrombus. 

The  condition  is  to  be  distinguished  from  pulmonary  tuberculosis 
largely  by  the  absence  of  tubercle  bacilli  and  the  location  of  the  signs  at 
the  bases  rather  than  the  apices  of  the  lungs.  In  addition  more  than  one 
area  may  be  involved  in  cases  of  infarction.  If  the  infarct  is  deeply 
seated  and  does  not  give  rise  to  physical  signs,  the  differentiation  may 
be  very  difficult. 

Owing  to  the  sudden  onset  of  the  symptoms  with  dyspnea,  pain  in 
the  side  and  bloody  sputum,  a  pulmonary  infarct  may  be  mistaken  for 
lobar  pneumonia.  In  the  case  of  an  infarct  an  initial  chill  is  rare;  fever 
may  not  appear  immediately,  and  when  present  does  not  resemble  that 
seen  in  pneumonia.  The  sputum  consists  of  liquid  blood  or  dark  red 
clots  and  is  not  viscid. 

In  malignant  disease  of  the  lungs  the  sputum  sometimes  consists  of 


DISEASES    OF    THE    LUNGS  475 

dark  clots  resembling  currant  jelly.  The  presence  of  a  primary  tumor 
elsewhere  should  make  the  cause  of  the  blood  spitting  apparent.  In 
any  event  the  course  of  the  disease  will  not  be  that  of  infarction  which 
tends  to  recovery. 

PULMONARY    CONGESTION 

The  term  pulmonary  congestion  is  loosely  applied  to  a  hyperemic  con- 
dition which  accompanies  or  follows  other  morbid  conditions  affecting 
the  lungs  or  heart.     Two  forms  are  described — the  acute  and  the  passive. 

ACUTE  CONGESTION 

Etiology. — Hyperemia  of  the  pulmonary  tissue  may  occur  in  a  variet3r 
of  conditions.  It  constitutes  part  of  the  pathological  picture  in  all  acute 
inflammatory  affections  of  the  lungs,  especially  the  first  stage  of  lobar 
pneumonia.  It  is  also  noted  in  varying  degrees  in  the  pulmonary  tissue 
surrounding  recent  tuberculous  deposits. 

Severe  overexertion  is  sometimes  attended  by  an  intensely  hyperemic 
condition  of  the  lungs  which,  in  a  few  instances,  has  been  believed  to  be 
the  cause  of  sudden  death  following  athletic  competition. 

Areas  of  acute  pulmonary  congestion  are  sometimes  noted  in  associa- 
tion with  the  acute  fevers,  notably,  typhoid,  influenza  and  malaria. 

A  very  frequent  cause  of  acute  pulmonary  congestion  is  the  inhalation 
of  irritant  gases.  If  the  exposure  is  slight,  recovery  ensues  but  if  the 
individual  is  subjected  to  a  large  dose  of  the  gas,  death  very  frequently 
ensues.  Oliver  has  noted  intense  congestion  of  the  lungs  as  the  result 
of  the  inhalation  of  carbon  monoxide  and  sulphuretted  hydrogen  gases 
and  from  the  fumes  of  nickel  and  ferri  carbonyl  and  nitrous  and  nitric 
acid.  He  has  also  called  attention  to  the  fact  that  a  workman  who  inhales 
chemical  fumes  may  not  exhibit  any  symptoms  immediately,  and  yet 
within  24  to  48  hours  he  dies  of  acute  congestion  of  the  lungs.  During 
the  present  European  war  chlorin  or  bromin  gas  has  been  used  exten- 
sively as  an  offensive  weapon.  The  effects  produced  by  the  inhalation 
of  irritant  gases  are  described  on  page  480. 

Exposure  to  extreme  cold  or  the  inhalation  of  very  hot  air  may  give 
rise  to  congestion  of  the  lungs. 

Woillez  has  described  a  primary  form  of  pulmonary  congestion  which 
occurs  without  known  cause.  While  the  existence  of  a  primary  form  is 
strongly  supported  by  French  writers,  most  authorities  do  not  recognize 
it.  The  onset,  the  symptoms  and  the  physical  signs  are  similar  to  those 
occurring  in  lobar  pneumonia  and  it  is  more  than  likely  that  it  represents 
a  mild  or  abortive  type  of  the  latter  disease.  It  has  a  duration  of  but 
four  or  five  days  and  almost  invariably  terminates  in  recovery. 

Morbid  Anatomy. — The  amount  of  blood  in  the  pulmonary  vessels 
depends  on  the  physiological  activity  of  the  lungs.  Hyperemia  may 
occur  under  normal  conditions.  If,  however,  a  hyperemic  condition 
arises  as  the  result  of  abnormal  conditions,  it  constitutes  a  congestion. 

Congestion  of  the  lungs  is  the  initial  stage  of  an  inflammatory  process 
and  is  usually  followed  by  an  exudation.     It  is  not  always  easy,  there- 
fore, to  draw  a  line  between  what  constitutes  simple  congestion  and  that 
which  may  be  considered  edema.     Acute  congestion  may  be  bilateral- 
or  it  may  be  limited  to  one  lung  or  a  portion  of  one  lung.     The  involved 


476         DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

portion  contains  an  excess  of  blood  clue  to  the  distended  capillaries.  On 
section  the  lung  resembles  what  may  be  seen  after  death  from  pneu- 
monia, when  the  disease  has  involved  parts  which  are  crepitant  and  not 
yet  consolidated.  The  affected  areas  are  bright  red,  crepitant,  feel  dry 
to  the  touch  and  there  is  very  slight  if  any  perceptible  increase  of  specific 
gravity. 

Symptoms. — Pulmonary  congestion  usually  gives  rise  to  some  dyspnea, 
cough  and  the  expectoration  of  frothy,  viscid  or  mucopurulent  material. 
The  sputum  may  be  streaked  with  blood  or  show  the  presence  of  red 
blood  cells  microscopically.  Unless  the  congestion  is  marked  and  as- 
sociated with  a  slight  amount  of  exudate,  the  sputum  may  be  very 
scanty  or  entirely  absent.  Congestion  due  to  the  inhalation  of  irritant 
gases  produces  the  most  marked  symptoms  and  in  addition  to  the 
dyspnea  and  cough,  there  are  marked  irritation  of  the  upper  respiratory 
tract  and  a  feeling  of  soreness  and  contraction  in  the  chest. 

PASSIVE  CONGESTION 

Etiology. — The  underlying  cause  of  passive  congestion  is  to  be  found, 
almost  invariably,  in  some  cardiac  affection.  Probably  the  most  com- 
mon form  of  congestion  of  the  lungs  is  that  known  as  hypostatic.  It  is 
very  frequently  present  at  the  bases  of  the  lungs  in  individuals  who  have 
been  confined  to  bed  for  a  long  time  because  of  some  protracted  febrile 
disease,  such  as  typhoid  or  other  long  debilitating  illness.  It  may  occur 
also  in  association  with  cerebral  lesions,  notably  those  which  produce 
paralysis  or  coma.  It  is  occasionally  encountered  in  cases  of  morphine 
poisoning.  Two  factors  enter  into  the  causation  of  hypostatic  conges- 
tion, namely,  a  weakened  heart  muscle  and  gravity.  That  a  weakened 
heart  muscle  is  the  chief  cause  is  evident  from  the  fact  that  a  healthy 
individual  may  lie  in  bed  for  an  indefinite  period  without  developing 
circulatory  disturbance  in  the  lungs. 

Another  form  of  passive  congestion  is  that  due  to  prolonged  stasis  of 
the  blood  in  the  pulmonary  circulation.  A  weak  heart  muscle,  whether 
it  be  due  to  myocarditis  or  dilatation  secondary  to  valvular  disease,  leads 
to  interference  with  the  return  of  the  blood  from  the  lungs  to  the  heart. 
Although  any  form  of  cardiac  disease  may  cause  passive  congestion,  the 
most  extreme  grades  of  the  condition  are  seen  in  cases  of  mitral  stenosis. 

Passive  congestion  is  sometimes  encountered  as  the  result  of  obstruc- 
tion to  the  flow  of  blood  through  the  pulmonary  capillaries.  Under  those 
circumstances  it  is  often  encountered  in  cases  of  chronic  emphysema  and 
fibroid  affections  of  the  lungs.  Thrombosis  of  the  pulmonary  veins  or 
compression  of  the  pulmonary  veins  by  an  aneurism  or  tumor  may  also 
produce  the  condition. 

Morbid  Anatomy. — Hypostatic  congestion  occurs,  as  a  rule,  in  the 
posterior  portions  of  the  bases  of  the  lungs  or  in  the  dependent  portion 
of  one  lung  if  the  patient  has  lain  on  that  side.  The  affected  portion  is 
dark  red  or  purplish  red  in  color,  heavier  than  normal  and  on  section 
drips  blood  or  bloody  serum.  Owing  to  the  fact  that  there  are  commonly 
associated  with  the  congestion  varying  degrees  of  edema  the  lung  pits  on 
pressure. 

In  those  cases  in  which  the  engorgement  of  the  blood-vessels  is  marked 
and  there  is,  in  addition,  some  leakage  of  the  blood  into  the  vesicles,  the 


DISEASES    OF    THE    LUNGS  477 

condition  is  sometimes  referred  to  as  hypostatic  pneumonia  or  spleniza- 
tion  of  the  lung. 

A  lung  which  has  been  the  seat  of  a  passive  congestion  due  to  stasis, 
of  long  standing,  is  somewhat  enlarged,  is  less  elastic  and  cuts  with 
greater  resistance  than  normal.  It  is  of  a  dark  red  or  purplish-red  color 
and  on  section  is  found  to  be  full  of  blood  of  a  venous  color.  The  en- 
gorged condition  of  the  lung  is  due  to  stasis  of  the  blood  current  in  the 
pulmonary  circulation.  In  mitral  stenosis,  for  instance,  the  pulmonary 
vessels  are,  on  the  one  hand,  distended  with  blood  which  is  dammed 
back  owing  to  the  obstruction  at  the  mitral  orifice,  and  on  the  other  hand, 
by  blood  which  is  forcibly  driven  into  them  by  the  hypertrophied  right 
ventricle.  This  gradually  leads  to  a  proliferation  of  the  fibrous  tissue  in 
the  septa  of  the  lung.  If  the  condition  persists,  the  continued  tension 
within  the  capillaries  leads  to  the  escape  of  red  blood  cells  by  diapedesis. 
The  blood  cells  eventually  break  down  and  liberate  the  blood  pigment. 
This  produces  a  condition  known  as  brown  induration  or  "heart  lung." 
In  such  a  lung  there  is  a  marked  increase  in  the  fibrous  tissue  and  the 
organ  is  of  a  dark,  rusty  brown  color.  On  section  a  brownish  colored 
fluid  can  be  squeezed  out.  Microscopically  this  fluid  is  seen  to  contain 
large  mononuclear  cells  containing  brownish  pigment.  These  cells, 
sometimes  referred  to  as  "heart  failure"  cells,  may  be  found  in  the 
sputum  also.  In  common  with  other  forms  of  pulmonary  fibrosis  there 
may  be  some  dilatation  of  the  bronchi. 

Symptoms. — There  are  no  symptoms  which  are  characteristic  of 
hypostatic  congestion.  It  may  give  rise  to  some  dyspnea,  slight  cyano- 
sis and  cough.  As  a  rule,  its  presence  is  detected  in  the  routine  examina- 
tion of  patients  suffering  from  typhoid  fever  or  other  adynamic  disease. 

Passive  congestion  due  to  heart  disease  does  not  produce  symptoms 
so  long  as  cardiac  compensation  is  maintained.  The  sputum,  however, 
may  show  the  presence  of  the  characteristic  pigmented  "heart  cells." 
The  first  evidence  of  failing  compensation  may  be  the  appearance  of 
dyspnea  and  cough,  especially  after  the  slightest  exertion.  Sputum  may 
be  absent  or  moderate  in  amount  and  when  present  may  be  blood- 
streaked.  Small  hemoptyses  may  occur  also.  Sudden  weakening  of 
the  left  ventricle  may  be  followed  very  quickly  by  marked  dyspnea, 
cyanosis,  cough  and  the  expectoration  of  blood-streaked  sputum.  The 
condition  is  often  referred  to  as  "cardiac  asthma." 

Physical  Signs.- — In  the  presence  of  hypostatic  congestion  examina- 
tion of  the  lower  and  posterior  portion  of  the  lungs  will  usually  show  some 
impairment  of  the  percussion  note,  more  or  less  suppression  of  the 
respiratory  murmur  and  the  presence  of  medium-sized  and  crepitant 
rales. 

Passive  congestion  due  to  heart  disease  does  not  give  rise  to  physical 
signs  unless  cardiac  compensation  fails.  In  the  event  of  this  happening 
mixed  rales  are  heard  over  both  lungs  especially  at  the  bases. 

Pulmonary  Edema 

This  condition  is,  as  a  rule,  a  sequel  of  congestion  and  differs  from 
the  latter  only  in  the  exudation  which  is  present.  Like  congestion, 
edema  occurs  in  an  acute  and  a  chronic  form. 

The  cause  of  pulmonary  edema  is  not  altogether  clear.     The  generally 


478         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

accepted  belief  is  that  the  exudate  arises  as  the  result  of  a  mechanical 
defect  which  is  cardiac  in  origin.  This  conception  is  based  on  the  classic 
experiments  of  Welch  who  believed  that  the  edema  resulted  from  stasis 
due  to  increased  capillary  tension.  The  tension  is  brought  about 'by  an 
excessive  amount  of  blood  in  the  pulmonary  capillaries,  due,  in  part,  to 
a  weakened  left  ventricle  which  dams  the  blood  back,  and,  in  part,  to  an 
excess  of  blood  forced  out  of  the  right  ventricle.  As  a  result  of  this  over- 
filling of  the  pulmonary  vessels,  serum  escapes  from  the  distended  capil- 
laries. This  explanation  is  entirely  applicable  to  the  so-called  terminal 
edema  which,  for  the  most  part,  is  associated  with  cardiac  or  cardiorenal 
disease. 

Sahli  attributes  the  edema  to  changes  in  the  capillary  vessels.  This 
hypothesis  is  supported  by  Krehl  who  points  out  that  the  edema  is 
unevenly  distributed  and  often  definitely  associated  with  inflammatory 
processes.  It  is  well  known  that  it  is  often  difficult  and  may  be  im- 
possible, to  distinguish  between  areas  of  edema  and  pneumonic  patches. 
Weakening  of  the  capillary  walls  may  be  produced  either  by  a  chronic 
disease  such  as  nephritis  or  by  an  acute  inflammatory  process. 

Edema  may  occur  also  after  general  anesthesia  or  in  the  course  of 
one  of  the  acute  infectious  diseases.  In  these  cases  it  is  believed,  by  some, 
that  the  edema  is  toxic  in  origin  especially  in  those  cases  in  which  there 
is  no  associated  cardiac  lesion  to  account  for  the  condition.  In  support 
of  this  view  is  the  well-known  fact  that  experimentally  the  injection  of 
adrenalin  will  produce,  in  animals,  a  condition  comparable  to  the  acute 
edema  seen  in  human  beings.  Recently  Kraus1  from  experimental  ob- 
servations, states  that  disturbance  of  the  nervous  mechanism  governing 
the  pulmonary  circulation  may  produce  edema. 

"On  the  whole,  the  most  acceptable  view  as  to  the  etiology  of  pul- 
monary edema  is  that  it  is  due  to  increased  capillary  tension  accompanied, 
aided,  and  probably  in  many  instances  preceded,  by  degenerative  changes, 
toxic  in  character,  of  the  capillary  endothelium"  (Hare). 

CHRONIC  PULMONARY  EDEMA 

Etiology.- — Localized  pulmonary  edema  is  met  with  under  a  variety  of 
conditions.  Occurring  in  the  pulmonary  tissue  surrounding  circumscribed 
lesions,  it  forms  part  of  the  pathological  picture  in  broncho-pneumonia, 
abscess,  new  growths,  infarcts  and  tuberculosis.  General  edema  of  the 
lungs  often  occurs  in  chronic  conditions,  such  as  cardiac  disease,  nephritis, 
anemia,  and  cerebral  disease.  As  a  terminal  event  it  is  not  uncommon. 
Cohnheim  has  said  of  this  type  that  patients  do  not  die  because  of  the 
edema,  but  the  edema  develops  because  the  patient  is  dying.  In  the 
great  majority  of  cases  the  terminal  edema  is  due  to  cardiac  failure. 
Coplin  found  that  cardiac  disease  was  the  cause  of  the  terminal  edema  in 
350  of  405  cases  in  which  the  condition  was  found  at  autopsy. 

Morbid  Anatomy. — General  pulmonary  edema  is  usually  bilateral 
and  most  marked  at  the  bases  of  the  lungs.  If,  however,  the  patient 
lies  constantly  on  one  side  the  edema  may  be  limited  to  the  dependent 
lung.  The  condition  is  sometimes  referred  to  as  hypostatic  pneumonia. 
The  affected  portion  is  heavier  than  normal,  pits  on  pressure  and  except 
in  extreme  cases,  is  slightly  crepitant.     On  section  the  involved  portion 

1  Bed.  Klin.  Woch.,  i,  1035,  1913. 


DISEASES    OF   THE    LUNGS  479 

is  pale  unless  there  has  been  marked  congestion,  when  the  cut  surface 
is  reddish  in  color.  The  cut  surface  may  present  a  glistening  gelatinous 
appearance  if  the  edema  is  extensive. 

The  characteristic  feature  is  the  outpouring  of  a  serous  exudate  into 
the  alveoli  and  interstitial  tissues.  When  the  lung  is  incised  there  pours 
out  a  clear,  frothy  serum.  If,  however,  congestion  has  been  marked  the 
serum  is  of  a  pinkish  or  reddish  color. 

Symptoms  and  Physical  Signs. — The  symptoms  are  essentially  the 
same  as  those  encountered  in  chronic  congestion.  In  patients  suffering 
from  a  prolonged  illness,  examination  of  the  bases  of  the  lungs  posteriorly 
will  often  show  impairment  or  even  absolute  dulness  of  the  percussion 
note;  suppression  of  or  absent  breath  sounds;  diminished  voice  sounds; 
and  fine  rales.  If  the  edema  is  extensive,  the  air  cells  and  bronchi  may 
be"; filled  with  the  exudate.  In  such  cases  rales  are  absent,  the  percussion 
note  is  dull  and  the  breath  and  voice  sounds  very  distant.  The  condi- 
tion may  be  mistaken  for  a  pleural  effusion.  The  introduction  of  a 
needle  is  often  needed  to  determine  the  presence  or  absence  of  fluid. 

ACUTE  PULMONARY  EDEMA 

This  condition  is  rarely  if  ever  primary  in  origin.  It  is  most  com- 
monly encountered  in  individuals  suffering  from  some  form  of  cardio- 
vascular disease,  particularly  angina  pectoris  and  myocarditis,  or  chronic 
Bright's  disease  associated  with  marked  arterial  hypertension.  Less 
frequently  it  is  met  with  in  association  with  some  one  of  the  acute  infec- 
tions, pregnancy,  epilepsy,  anesthesia,  or  as  one  of  the  manifestations  of 
angio-neurotic  edema.  A  few  cases  have  been  recorded  in  which  the  con- 
dition followed  the  removal  of  a  pleural  or  abdominal  effusion.  Acute 
pulmonary  edema  may  end  fatally  in  a  few  hours;  on  the  other  hand, 
there  may  be  a  succession  of  attacks  occurring  at  more  or  less  frequent 
intervals  for  years.  Two  cases  which  have  come  to  my  notice  have 
had  repeated  attacks,  one  because  of  the  associated  external  phenomena 
was  undoubtedly  angio-neurotic  in  origin;  the  other  while  apparently 
idiopathic,  had  in  all  probability,  a  similar  basis. 

Morbid  Anatomy. — In  those  cases  in  which  a  fatal  issue  has  occurred, 
the  lungs  are  found  to  be  heavy,  water-logged  and  pit  on  pressure.  When 
cut,  an  excessive  amount  of  clear  or  pinkish-colored  serum  exudes. 

Symptoms. — The  onset  is  sudden,  with  a  feeling  of  oppression  in  the 
chest,  extreme  dyspnea  or  even  orthopnea,  and  a  short,  incessant  cough. 
Large  quantities  of  clear  or  faintly  blood-tinged,  frothy  serum  are  expec- 
torated. In  extreme  cases  the  frothy  serum  may  be  expelled  in  a  sudden 
gush  through  both  the  mouth  and  nose.  In  individuals  suffering  from 
chronic  cardiac  or  renal  disease  the  pulse  is  very  weak,  and  it  is  in  these 
cases  that  a  fatal  issue  is  to  be  feared.  The  labored  breathing,  the  cyano- 
sis, and  above  all,  the  character  of  the  expectorated  material  renders  the 
diagnosis  easy  almost  at  a  glance. 

Physical  Signs. — There  are  no  signs  especially  characteristic  of  this 
condition. 

Inspection. — Aside  from  the  labored  character  of  the  breathing,  there 
are  no  noteworthy  signs  referable  to  the  chest. 

Palpatio?!  may  reveal  a  rhonchal  fremitus,  although  this  is  not  apt 
to  be  the  case,  as  the  rales  are  of  the  fine  sibilant  and  subcrepitant  type. 


480         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Percussion  is  negative,  except  in  the  fatal  cases  where  the  outpouring 
of  the  serum  is  so  great  as  to  produce  impairment  of  the  pulmonary 
resonance. 

Auscultation. — The  breath  sounds  are  for  the  most  part  obscured  by 
the  numerous  fine  sibilant  and  fine  bubbling  rales.  The  heart  sounds  are 
obscured  for  the  same  reason,  and  also  because  of  weakness  on  the  part 
of  the  heart  itself. 

Effects  of  poisonous  Gases  on  the  Respiratory  Tract 

The  rapidity  with  which  poisonous  gases  act  when  inhaled  can  be 
readily  understood  when  there  is  taken  into  consideration  the  fact  that 
they  are  diffused  in  the  same  manner  as  the  respired  air  and  hence  come 
into  contact  with  the  enormous  absorptive  area  of  the  lungs  which 
includes  myriads  of  capillaries.  Oliver1  states  that  poisonous  gases  are 
of  two  kinds:  (1)  the  purely  toxic,  illustrated  by  carbon  monoxide;  and 
(2)  irrespirable  gases,  as  for  instance,  chlorin,  bromin,  etc.  Both  kinds 
cause  asphyxia.  The  first  interfere  with  the  respiratory  function  by 
acting  as  a  direct  poison  to  the  red  blood  corpuscles  rendering  them  unfit 
for  taking  up  oxygen;  the  second  by  irritating  or  destroying  the  mucous 
membrane  of  the  air  tubes  and  the  alveoli. 

Toxic  gases,  such  as  carbon  monoxide,  illuminating  gas,  water  gas, 
etc.,  manifest  themselves  chiefly  by  their  effects  on  the  nervous  system. 
The  milder  symptoms  consist  of  giddiness,  headache,  throbbing  temples 
and  ringing  in  the  ears.  In  the  severe  cases  a  profound  narcosis  may 
develop  from  which  there  may  be  no  awakening.  Oliver  has  observed 
cases  in  which  there  was  neither  immediate  irritation  of  the  lungs  caused  by 
the  inhalation  of  carbon  monoxide  nor  marked  difficulty  of  breathing, 
yet  a  few  days  after  an  apparent  recovery  death  may  come,  preceded  by 
signs  of  acute  congestion  of  the  lungs. 

So  far  as  the  respiratory  tract  is  concerned  our  chief  interest  is  with 
the  irrespirable  gases.  The  effects  of  these  gases  have  attracted  con- 
siderable notice  during  the  past  two  years  owing  to  their  use  as  an  offen- 
sive weapon  in  the  European  war. 

Etiology. — In  civil  life  nitrous  and  nitric  acid  fumes  are  the  ones 
which  most  frequently  cause  trouble.  The  inhalation  of  these  fumes 
may  occur  in  laboratories  or  factories  in  which  considerable  quantities 
of  these  gases  are  formed  either  during  the  course  of  some  reaction  or 
when  a  carboy  of  nitric  acid  is  spilled.  Wood2  in  reporting  a  personal 
observation  with  autopsy  findings,  has  collected  nine  similar  cases.  In 
addition  he  found  in  the  literature  references  to  a  very  considerable 
number  in  which  respiratory  symptoms  were  severe  but  in  which  the 
autopsy  reports  were  incomplete  or  wanting.  Exposure  to  the  fumes 
may  occur  in  a  variety  of  ways  and  one  or  a  number  of  individuals  may 
be  simultaneously  affected.  Pott3  reports  an  instance  in  which  thirty 
individuals  were  exposed  to  nitrogen  tetroxide  fumes  formed  by  the 
action  of  acid  phosphate  on  sodium  nitrate  in  the  preparation  of  a 
fertilizer.  There  were  two  deaths  and  in  addition  eight  more  indi- 
viduals were    confined  to  bed  for  a  number  of  days  with  severe  respi- 

1  "Diseases  of  Occupation,"  1908. 

2  Trans.  Assoc.  Am.  Phys.,  1912. 

3  Deut.  Med.  Woch.,  1884,  x,  451. 


DISEASES    OF   THE    LUNGS  481 

ratory  symptoms  (dyspnea,  cough  and  the  expectoration  of  thick 
yellow  sputum  containing  blood).  Hall  and  Cooper1  report  a  similar 
experience  in  which  twenty  people  were  exposed  to  nitric  acid  fumes. 
In  this  instance  a  carboy  of  nitric  acid  was  broken  and  in  spreading  over 
the  floor  attacked  some  zinc  plates  and  sawdust,  starting  a  fire.  All 
developed  marked  respiratory  symptoms  and  four  died.  Exposure  to 
nitrous  fumes  also  occurs  among  those  engaged  in  the  manufacture  of 
explosives  and  those  exposed  to  the  fumes  which  follow  blasting  or  the 
explosion  of  shells.  In  mines  where  dynamite,  gelignite  and  nitro- 
explosive  compounds  are  used  the  fumes  given  off  from  the  explosives 
may  travel  to  other  portions  of  the  mine  and  affect  the  men  working 
there  or  the  men  may  return  to  the  scene  of  the  blasting  too  soon  after 
the  explosion  has  occurred.  Macaulay  and  Irvine2  state  that  in  the 
year  1904-1905  40  deaths  were  due  to  "gassing"  in  the  South  African 
mines  and  of  this  number  17  were  caused  by  nitrous  fumes.  The  diag- 
nosis was  confirmed  by  autopsy  in  one-half  the  cases.  Ohnesorg3  states 
that  following  the  explosion  of  modern  shells  there  is  liberated  carbon 
monoxide  or  nitrogen  monoxide  or  both.  The  latter  as  the  result  of 
chemical  changes  is  converted  into  nitrous  and  nitric  acids. 

Among  the  less  common  irrespirable  gases  may  be  mentioned  nickel 
carbonyl,  ferri  carbonyl  and  sulphuretted  hydrogen  gas.  Nickel  and 
ferri  carbonyl  are  both  very  volatile  liquids,  the  fumes  of  which  are 
extremely  poisonous. 

Although  chlorin  gas  has  long  been  known  to  be  an  intense  respira- 
tory irritant  but  little  attention  was  paid  to  it  until  its  introduction  as 
an  offensive  weapon  in  the  present  war.  The  term  "gassing,"  so  fre- 
quently employed  of  late,  is  not  a  product  of  the  war  but  has  long  been 
used  by  workers  in  chemical  factories.  The  gas  is  very  irritant  to  the 
respiratory  tract  and  men  engaged  in  the  manufactuie  of  bleaching 
powder,  for  instance,  can  bear  exposure  to  the  fumes  for  not  more  than 
half  an  hour.  Even  then  it  is  necessary  to  protect  the  eyes  with  goggles 
and  to  cover  the  mouth  with  some  material  which  will  prevent  the  in- 
halation of  the  fumes.  It  is  said,  however,  that  chlorin  workers  acquire 
considerable  tolerance  and  can  withstand  gas  in  concentration  that 
would  produce  glottic  spasm  in  the  untrained.  Bromin  in  its  action 
is  similar  to  chlorin  but  less  severe.  The  fumes  from  hydrochloric 
acid  are  also  very  irritating  to  the  respiratory  tract. 

Oliver  states  that  taking  chemical  workers  as  a  whole  it  may  be  said 
that  the  younger  men  are  not  an  unhealthy  class.  The  continued  ex- 
posure to  irritating  gases,  however,  eventually  renders  them  subject 
to  bronchitis,  asthma,  and  other  respiratory  troubles. 

Morbid  Anatomy. — The  action  of  all  the  irrespirable  gases  on  the 
respiratory  tract  is  essentially  the  same,  namely,  that  of  an  intense 
irritant.  The  extent  of  the  damage  depends,  of  course,  on  the  severity 
of  the  exposure.  In  severe  cases  the  lungs  are  found  at  autopsy  to  be 
voluminous  and  very  heavy,  sometimes  three  or  four  times  their  normal 
weight.  On  section  they  are  found  to  be  intensely  congested,  edematous, 
and  of  a  general  reddish  color.  In  addition  there  is  a  patchy  distribution 
of  small  granular  areas  which  are  bright  red  or  reddish-brown  in  color. 

1  Jour.  Am.  Med.  Assoc,  1905,  xlv,  390. 

2  Quoted  by  Oliver. 

3  U.  S.  Naval  Bulletin,  October,  1910. 

31 


482  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

These  areas  are  always  suggestive  of  the  action  of  a  toxic  gas  (Oliver). 
If  the  patient  survives  for  several  days  there  may  be  also  areas  of  broncho- 
pneumonia. Fauntleroy1  states  that  following  the  inhalation  of  chlorin 
gas  the  air  cells  are  often  enormously  dilated  and  that  these  may  be  filled 
with  a  thin,  watery,  and  sometimes,  blood-streaked  mucus.  Patches 
of  fibrinous  pleurisy  may  be  present.  The  mucous  membrane  of  the 
bronchial  tree  is  congested,  edematous  and  shows  a  loss  of  epithelium. 
The  walls  of  the  bronchi  may  be  edematous  also.  Edema  of  the  larynx 
is  often  present  and  in  some  instances  is  the  immediate  cause  of  death. 

Microscopically  some  of  the  air  cells  are  narrowed,  others  are  greatly 
increased  in  size  and,  in  other  instances,  there  may  be  a  fusion  of  a  number 
of  alveoli  forming  large  open  spaces.  The  alveoli  contain  a  serous  or 
fibrinous  exudate,  red  and  white  blood  cells  and  desquamated  epithelium. 
Numerous  thrombi  are  seen  in  the  smaller  vessels. 

As  the  result  of  experimental  observations  on  the  effect  of  chlorine 
gas  Schafer2  concludes  that  a  fatal  result  is  brought  about  by  obstruction 
in  the  pulmonary  blood-vessels  and  not  by  constriction  of  the  bronchioles. 
In  "gassed"  animals  the  pulmonary  capillaries  are  seen,  microscopically, 
to  be  gorged  with  blood,  and,  presumably  as  a  result  of  this  stasis,  there 
is  marked  edema  of  the  interstitial  tissue  of  the  lungs.  Similar  results 
were  obtained  by  Wood3  from  the  experimental  use  of  nitrogen  tetroxide. 
As  a  result  of  the  thrombi  and  stasis  in  the  pulmonary  vessels  the  work 
of  the  heart  is  increased  tremendously.  For  this  reason  death  from 
cardiac  failure  is  common,  the  heart  becoming  exhausted  in  trying  to 
pump  the  blood  through  the  engorged  capillaries  surrounding  the  bron- 
chioles and  alveoli.  Pojarsky4  in  a  study  of  40  cases  found  that  serious 
complications  may  evolve  after  three  days  in  the  shape  of  putrid 
bronchitis,  gangrene  or  pulmonary  emboli  and  infarcts. 

If  the  case  is  only  moderately  severe  and  recovery  takes  place,  a 
chronic  bronchitis  may  persist,  or  patches  of  fibrosis  eventually  may 
appear  in  the  lungs.  Bronchiectasis  is  cited  by  Fauntleroy5  as  one  of  the 
sequels.  An  interesting  sequel  to  the  inhalation  of  an  irritant  gas  is 
bronchiolitis  fibrosa  obliterans.  This  is  considered  under  a  separate 
heading  (see  p.  265). 

Symptoms. — In  the  case  of  chlorin  and  bromin,  especially  the 
former,  the  first  effect  is  to  cause  the  eyes  to  water.  This  is  quickly 
followed  by  violent  irritation  of  the  bronchial  tract.  If  the  exposure 
has  been  severe,  an  intense  inflammation  of  the  capillary  bronchi  is  set 
up  associated  with  a  hypersecretion  of  thin  watery  mucus,  which  fills 
up  the  air  spaces  of  the  lungs  and  practically  causes  death  by  drowning. 
When  the  concentration  of  the  gas  is  not  so  marked  the  initial  symptoms 
are  less  severe.  Hill6  has  given  an  excellent  description  of  the  symptoms 
in  these  cases.  The  temperature  is  subnormal,  the  pulse  full  and  strong, 
except  in  case  of  collapse,  the  face  is  cyanosed  and  the  expression  anxious. 
The  patient  often  assumes  a  sitting  posture  and  gasps  for  air.  In  other 
instances  he  lies  with  the  head  hanging  over  the  edge  of  the  stretcher 
"or  bed  to  aid  in  getting  rid  of  the  sputum.     The  respirations  are  jerky 

1  Report  on  the  Medico-Militarv  Aspects  of  the  European  War,  etc.,  1915. 

2  Brit.  Med.  Jour.,  Aug.  14,  1915. 

3  hoc.  cit. 

4  Russky  Vratch.,  No.  28,  1915. 

5  hoc.  cit. 

6  Brit.  Med.  Jour.,  Dec.  4,  1915. 


DISEASES    OF    THE    LUNGS  483 

and  hurried,  and  associated  with  a  choking  cough  and  varying  amounts 
of  frothy  expectoration.  With  each  inspiration  the  chest  is  expanded 
to  its  fullest  capacity  and  all  the  auxiliary  muscles  of  respiration  are 
brought  into  play  as  in  an  asthmatic  paroxysm.  This  is  the  first  or 
asphyxial  stage,  which  if  the  patient  survives  passes  off  in  about  36  hours. 
After  a  few  hours  of  comparative  quiet  the  evidences  of  bronchitis  appear 
and  if  the  patient  survives  this  there  is  a  quiescent  period  followed  by 
intense  bronchitis.  The  frothy  sputum  becomes  greenish  in  color, 
fever  develops,  the  pulse  becomes  feeble  and  rapid  and  the  respirations 
hurried,  shallow  and  choking  in  character. 

In  warfare  the  concentration  of  the  gas  varies  owing  to  the  capricious 
action  of  the  wind  in  distributing  it.  The  symptoms  manifested  by  the 
men  vary,  therefore,  from  the  grave  cases  which  are  cyanosed  and  gasping 
for  breath  to  those  suffering  from  a  mild  form  of  irritation  of  the  bron- 
chioles. As  a  result  recovery  is  quick  in  some,  a  fatal  issue  occurs  at 
once  or  in  a  few  days  in  others,  while  in  still  others  recovery  is  followed 
by  some  permanent  damage. 

The  symptoms  following  the  inhalation  of  nitrous  and  nitric  acid 
fumes  are  rarely  as  severe  as  those  following  exposure  to  chlorin.  If  the 
concentration  is  not  great  there  may  be  nothing  more  than  a  slight  cough 
and  an  acid  taste  in  the  mouth.  Even  when  the  concentration  is  marked 
there  may  be  no  immediate  ill  effects  but  24  or  48  hours  later  the  patient 
may  suddenly  develop  an  attack  of  acute  congestion  and  edema  of  the 
lungs,  preceded  by  an  abundant  expectoration  of  thin,  yellow  material. 
As  a  rule,  however,  exposure  to  concentrated  nitric  acid  vapors  is  fol- 
lowed immediately  by  a  sense  of  oppression  in  the  chest,  dyspnea,  cough, 
faintness  and  cyanosis.  After  reaching  the  fresh  air,  the  patient  may 
vomit  and  respiratory  symptoms  clear  up.  After  an  interval  of  6  or  8 
hours  the  patient  is  suddenly  seized  with  intense  dyspnea  and  a  sense  of 
oppression  in  the  chest,  the  eyes  protrude  and  a  cold  sweat  appears. 
The  attack  is  very  similar  to  an  asthmatic  seizure.  In  addition  there 
are  cyanosis  and  paroxysms  of  coughing  which  may  last  10  or  15  minutes. 
Death  occurs  in  consequence  of  edema  of  the  lungs  which  is  usually 
preceded  by  the  expectoration  of  frothy  yellow  fluid.  In  acute  cases 
death  may  occur  within  48  hours;  occasionally  the  patient  may  linger  on 
for  one  or  two  weeks. 

Men  who  have  been  exposed  to  the  fumes  of  nitrous  and  nitric  acid 
following  the  explosion  of  a  shell  may  not  be  affected  at  first.  Later  they 
develop  dyspnea,  thirst,  perspiration,  abnormal  heart  action,  and  anginal 
symptoms.  The  sputum,  at  first  lemon  yellow  in  color,  becomes  very 
fluid  and  is  tinged  with  blood.  Finally  cyanosis  becomes  marked.  When 
the  amount  of  the  gas  inhaled  has  been  small  there  may  be  slight  evi- 
dences of  edema  of  the  lungs,  which  are  followed,  after  some  days,  by  the 
symptoms  and  signs  of  bronchitis  or  lobar  pneumonia  or  lobular  pneu- 
monia. There  is  usually  marked  dyspnea,  cough  and  the  expectoration 
of  tenacious  yellowish  or  brown  colored  sputum.  Vomiting  may  be  ex- 
treme and  thus  distract  the  attention  from  the  lungs.  These  cases 
often  recover  but  show  a  decided  tendency  to  attacks  of  bronchitis  for 
some  time. 

Physical  Signs. — In  the  early  stages  the  physical  signs  are  those  of 
congestion  or  edema  of  the  lungs.  In  the  prolonged  cases  signs  of  lobar 
or  lobular  pneumonia  may  develop.     If  recovery  takes  place  the  lungs 


484         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

may  clear  up  entirely  or  there  may  be  the  physical  signs  of  a  chronic 
bronchitis,  bronchitis  obliterans,  bronchiectasis  or  pulmonary  fibrosis. 
Diagnosis. — It  is  of  considerable  medico-legal  importance  to  be  able 
to  determine  the  cause  of  the  pulmonary  congestion  and  edema.  A 
knowledge  of  the  occupation  is  the  most  important  fact.  It  is  also  to  be 
borne  in  mind  that  the  symptoms  of  pulmonary  damage  may  not  occur 
for  from  24  to  48  hours  after  the  exposure  to  the  gas  has  taken  place. 

Hydatid  Disease  of  the  Lung  and  Pleura 

Hydatid  disease  of  the  different  viscera  is  due  to  the  ovum  of  the 
Taenia  echinococcus  of  the  dog.  In  man  the  ovum  develops  into  the 
larva — the  hydatid — and  persists  in  that  state. 

Etiology. — Hyatid  disease  has  a  fairly  definite  geographical  distribu- 
tion. The  vast  majority  of  cases  have  been  reported  from  Iceland, 
Australia  and  the  Argentine.  Wherever  man  is  brought  into  intimate 
contact  with  infected  dogs  the  disease  is  relatively  common.  Dogs 
used  for  herding  sheep  are  a  common  source  of  infection  and  this  largely 
explains  the  frequency  of  the  disease  in  Australia  and  the  Argentine.  In 
this  country  sporadic  instances  of  the  disease  are  occasionally  encountered 
and  at  times  an  imported  case  is  seen. 

The  abdominal  viscera,  particularly  the  liver,  are  the  most  frequent 
sites  of  the  disease.  Among  1863  cases  of  hydatid  disease,  the  lung  or 
pleura  was  involved  in  153  or  8.3  per  cent.1  Thomas2  collected  809  cases 
from  the  Australian  Hospitals  and  of  this  number  the  lung  or  pleura  was 
involved  in  136,  or  16.8  per  cent.  In  a  series  of  952  cases  reported  from 
the  Argentine  by  Vagas  and  Cranwell3  the  lung  and  pleura  were  involved 
in  but  54  or  5.6  per  cent. 

The  sexes  are  equally  affected.  As  a  rule  the  disease  occurs  among 
the  lower  class. 

Morbid  Anatomy. — The  ovum  of  the  taenia  is  eliminated  with  the 
dog's  feces.  Infection  of  human  beings  may  be  brought  about  by  con- 
taminated food  or  drinking  water  or  by  the  hands  becoming  soiled  in 
petting  dogs.  Direct  infection  of  the  lung  through  the  inhalation  of  dust 
containing  the  ova  was  believed  by  Bird  of  Australia  to  be  a  possibility, 
but  this  theory  has  received  no  support. 

The  accepted  teaching  is  that  the  ovum  is  taken  into  the  stomach 
where  the  envelope  is  dissolved.  The  liberated  ovum  then  bores  through 
the  wall  of  the  stomach  or  intestines  and  in  the  majority  of  instances  is 
carried  by  the  portal  vein  to  the  liver.  Thus  in  1863  collected  cases  953 
or  51  per  cent,  the  disease  was  localized  in  the  liver.  How  the  ovum 
reaches  the  lung  is  not  clear.  In  many  instances  it  apparently  passes 
through  the  vessels  of  the  diaphragm  this  assumption  being  strengthened 
by  reason  of  the  fact  that  the  liver  is  so  frequently  involved  and  that  in 
addition,  the  right  lower  lobe  is  the  most  common  site  in  the  lungs.  In- 
volvement of  other  portions  of  the  respiratory  tract  probably  results 
from  the  ovum  entering  a  systemic  vein  and  eventually  reaching  the 
lungs  through  the  pulmonary  arteries.  Echinococcus  infection  of  the 
lungs  may  be  primary  or  secondary.     When  secondary  the  disease  may 

1  Combined  statistics  of  Davaine,  Cobbold,  Finsen  and  Neisser. 

2  "Hydatid  Disease,"  1894. 

3  Revue  de  Chir.,  vol.  xxiii,  970,  1901. 


DISEASES    OF    THE    LUNGS  485 

extend  from  the  liver  or  the  infection  may  arise  through  metastasis  from 
the  liver  or  some  other  organ.  Having  become  localized  in  the  pul- 
monary or  pleural  tissues  the  ovum  loses  its  hooks  and  is  gradually 
transformed  into  a  cyst.  The  cyst  wall  is  composed  of  a  stratified  or 
laminated  wall,  the  inner  layer  being  granular  or  parenchymatous  in 
character.  From  this  parenchymatous  layer  brood  capsules,  scoleces 
and  finally  daughter  cysts  may  develop. 

In  the  lungs  hydatid  disease  may  occur  in  the  form  of  a  single  cyst 
which  varies  considerably  in  size;  it  may  attain  the  dimensions  of  a 
fetal  head.  In  some  instances  the  cyst  is  multilocular  and  rarely 
numerous  small  cysts  may  be  scattered  throughout  the  lung.  When  the 
disease  is  located  in  the  pleura  it  usually  occurs  in  the  form  of  a  single 
cyst. 

The  contents  of  the  cyst  consist  of  a  clear,  transparent  fluid  contain- 
ing the  characteristic  hooklets.  In  some  instances  the  fluid  may  be 
sterile  or  as  the  result  of  secondary  infection  the  fluid  may  contain  pus. 

The  effect  of  the  cyst  is  that  of  an  irritant.  The  pulmonary  tissue 
about  it  may  become  congested  and  later  undergo  fibroid  changes.  In 
cases  of  long  standing  the  wall  is  apt  to  be  very  thick  and  fibrous.  The 
cyst  may  rupture  into  one  of  the  bronchi,  into  the  pleural  cavity  or^ 
rarely,  into  the  pericardium.  Rupture  into  a  bronchus  is  the  most  usual 
termination.  This  may  end  in  complete  recovery  but  if  the  wall  is 
thick  secondary  infection  and  gangrene  may  result.  Rupture  into  the 
pleural  cavity  is  usually  followed  by  a  fatal  result. 

Localization  of  the  echinococcus  in  the  pleura  is  not  common  and 
when  the  thoracic  organs  are  involved  it  is  the  lungs  that  are  usually 
affected.  All  statistics  bear  out  the  fact  that  the  right  lower  lobe  is 
involved  far  more  often  than  any  other  portion  of  the  lungs. 

Symptoms. — The  presence  of  a  cyst  in  the  lung  or  pleura  may  give 
rise  to  symptoms  during  the  early  stages  when  the  growth  is  small  or  if 
it  is  centrally  located  and  does  not  cause  pressure  symptoms.  As  long 
as  the  cyst  remains  intact  constitutional  symptoms  are  absent  and  the 
patient  presents  a  healthy  appearance.  As  the  cyst  increases  in  size, 
however,  a  dry,  hacking  cough  usually  occurs  and  this  may  be  accompanied 
by  mucoid  expectoration. 

The  most  important  symptom  is  hemoptysis.  This  is  the  most  fre- 
quent and  the  most  striking  symptom  of  the  disease  and  occurs  in  the 
majority  of  cases.  It  may  appear  as  an  early  manifestation;  during  the 
course  of  the  disease;  or  coincidently  with  rupture  of  the  cyst.  In 
common  with  tuberculosis  the  first  evidence  of  the  disease  may  be  blood 
spitting  and  as  Dieulafoy  has  well  expressed  it,  "the  first  cry  of  revolt 
on  the  part  of  the  lung  against  the  invader  is  perhaps  a  means  of  de- 
fense." In  the  early  stages  of  the  disease  the  hemorrhage  may  be  slight 
but  if  associated  with  rupture  of  the  cyst  the  bleeding  is  apt  to  be  profuse. 

Pain  may  or  may  not  be  present.  If  the  pleura  is  not  involved  either 
primary  or  secondary  pain  is  usually  absent.  There  may  be,  however,  a 
sense  of  weight  or  oppression  in  the  chest. 

Dyspnea  is  not  apt  to  be  a  feature  of  the  disease  unless  the  cyst  at- 
tains a  large  size.  Fever  is  not  apt  to  be  present  unless  there  has  been 
a  secondary  infection  of  the  cyst  contents  or  an  associated  inflammation 
of  the  lungs,  such  as  broncho-  or  croupous  pneumonia. 

Pressure  symptoms  will  depend  on  the  size  and  location  of  the  growth. 


486         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

They  are  not  common.  The  localization  of  the  disease  in  the  right 
lower  lobe  in  a  large  proportion  of  the  cases,  precludes  this  possibility. 
When  the  disease  is  so  situated  as  to  cause  pressure  symptoms  they  are 
identical  with  those  produced  by  tumors. 

Rupture  of  the  cyst  occurs  in  about  half  of  the  cases  and,  as  a  rule,  the 
rupture  occurs  into  a  bronchus.  Rupture  into  a  bronchus  is  attended 
by  a  violent  paroxysmal  cough,  urgent  dyspnea  and  pain  or  a  sense  of 
oppression  in  the  chest.  These  symptoms  are  accompanied  by  the  ex- 
pectoration of  a  large  quantity  of  clear  transparent  fluid.  In  some 
instances  there  may  be,  in  addition,  a  brisk  pulmonary  hemorrhage. 
Examination  of  the  expectorated  fluid  may  show  the  presence  of  the 
hydatid  hooklets  or  fragments  of  the  cyst  wall,  the  latter  resembling  the 
skins  of  grapes. 

Rupture  into  a  bronchus  may  be  followed  by  an  almost  immediate 
fatal  result.  The  evacuation  of  the  cyst  may  be  complete  in  a  few  days 
or  it  may  be  intermittent  and  extend  over  a  period  of  weeks.  If  the  cyst 
is  old  and  the  wall  has  become  thickened  secondary  infection  may  occur. 
This  gives  rise  to  a  purulent  expectoration  which  gradually  disappears. 
Gangrene  of  the  cyst  wall  and  surrounding  tissues  may  occur. 

Rupture  into  the  pleural  cavity  is  attended  by  the  sudden  onset  of 
severe  pain,  dyspnea  and  signs  of  shock  similar  to  those  encountered  in 
pneumothorax.  Rupture  into  the  pericardial  sac  produces  pain  in  the 
chest  and  serious  circulatory  disturbances. 

Physical  Signs. — Inspection.- — If  the  cyst  is  large  and  located  in  the 
pleura  or  near  the  periphery  of  the  lung  there  may  be  bulging  of  the  chest 
wall;  after  evacuation  retraction  may  be  noted.  Restriction  of  motion 
is  usually  noted  in  that  portion  of  the  chest  which  overlies  the  cyst. 
Pressure  signs  are  rare. 

Palpation. — This  may  reveal  slight  degrees  of  diminished  expansion. 
If  the  cyst  is  in  contact  with  the  chest  wall,  the  tactile  fremitus  will  be 
diminished. 

Percussion.- — If  the  cyst  is  in  contact  with  the  chest  wall  the  percus- 
sion note  over  it  is  absolutely  dull.  The  dulness  may  be  modified,  how- 
ever, if  a  thin  layer  of  pulmonary  tissue  intervenes.  If  the  cyst  is  situ- 
ated in  the  lower  part  of  the  chest,  the  dull  percussion  note  may  lead  to  a 
diagnosis  of  effusion.  In  the  case  of  a  cyst  the  upper  level  of  dulness  may 
be  in  front  or  in  the  axilla.  In  the  case  of  an  effusion  the  highest  point 
of  dulness  is  always  posterior  near  the  spine.  After  evacuation  the  per- 
cussion note  over  the  site  of  the  cyst  may  be  tympanitic  or  amphoric  in 
quality. 

Auscultation. — Over  the  site  of  the  cyst  the  breath  and  voice  sounds 
are  absent.  After  the  cyst  has  become  emptied  there  may  be  cavity 
signs:  cavernous  breathing,  whispering  pectoriloquy  and  metallic  rales. 
The  auscultatory  signs  surrounding  the  cyst  will  depend  on  whether 
inflammatory  changes  have  taken  place  in  the  pulmonary  tissue.  Noth- 
ing abnormal  may  be  heard  or  there  may  be  rales  and  an  alteration  in 
the  character  of  the  breath  sounds. 

Diagnosis. — In  countries  where  the  disease  is  endemic,  mistakes  in 
diagnosis  are  less  likely  to  occur  than  in  those  regions  where  an  occasional 
sporadic  case  is  seen.  Prior  to  rupture  of  the  cyst  it  is  not  possible  to 
make  an  absolutely  positive  diagnosis.  If  in  a  suspected  case  the  lesion 
is  unilateral,  basal  and  right-sided  and  in  addition  the  X-ray  examination 


DISEASES    OF   THE    LUNGS  487 

shows  a  globular  shadow,  echinococcus  disease  is  probably  present. 
After  rupture  of  the  cyst  the  diagnosis  is  much  easier.  The  location  of 
the  lesion  and  the  sudden  expectoration  of  a  large  quantity  of  clear  fluid 
is  highly  suggestive.  The  finding  of  the  hydatid  hooklets  or  fragments 
of  the  cyst  wall  is  the  only  means  of  being  absolutely  certain  of  the 
diagnosis. 

Echinococcus  disease  is  most  apt  to  be  confused  with  tuberculosis, 
a  pleural  effusion  or  a  thoracic  tumor. 

Tuberculosis  is  either  confined  to  the  summit  of  the  lung  or  if  the 
disease  involves  the  entire  lung  the  physical  signs  are  always  most  marked 
at  the  apex.  Although  hydatid  disease  may  involve  the  upper  portion 
of  the  lung  its  usual  location  is  at  the  right  base.  Tuberculosis  nearly 
always  causes  shrinkage  of  the  chest  wall  while  a  cyst  produces  bulging. 
A  hydatid  cyst  may  give  rise  to  marked  dulness  anteriorly  with  a  normal 
note  posteriorly  or  the  dulness  may  extend  across  the  middle  line. 

Active  tuberculosis  is  always  attended  by  constitutional  symptoms 
particularly  fever  and  loss  of  weight  while  a  hydatid  cyst  rarely  affects 
the  general  health  unless  secondary  infection  with  the  pus  cocci  or 
gangrene  develops  after  rupture. 

In  the  case  of  a  large  basal  cyst  the  condition  may  simulate  a  yleural 
effusion.  In  the  latter  the  line  of  dulness  is  always  higher  posteriorly 
near  the  spine,  there  may  be  movable  dulness  and  over  the  upper  limits 
of  the  effusion  egophony  is  commonly  heard.  Pain  or  tenderness  on 
pressure  is  common  in  pleurisy  and  is  often  absent  or  very  slight  in 
hydatid  cyst.  The  contour  of  the  shadow  in  the  X-ray  plate  may  serve 
to  distinguish  the  two  conditions,  that  of  the  cyst  being  globular  in 
outline. 

If  pressure  symptoms  are  present,  the  differentiation  between  a 
hydatid  cyst  and  a  malignant  tumor  may  be  difficult.  In  the  former 
constitutional  symptoms  are  slight  or  absent  while  in  the  case  of  the 
latter  the  evidences  of  a  rapid  decline  sooner  or  later  manifest  themselves. 

Pulmonary  Distomatosis 

Etiology. — This  affection  is  known  also  as  lung  fluke  disease,  parasitic 
hemoptysis,  endemic  hemoptysis  and  paragonimiasis.  The  disease  is 
deserving  of  some  attention,  for,  although  the  United  States  are  not 
included  in  its  geographical  distribution,  isolated  cases  are  apt  to  be 
encountered  at  any  time,  especially  among  those  who  have  resided  in  the 
far  East.  The  disease  occurs  in  Japan,  China,  and  Korea.  Among  the 
inhabitants  of  the  Island  of  Formosa  endemic  hemoptysis  is  very  prev- 
alent and  in  certain  districts  as  high  as  15  per  cent,  of  the  population  is 
said  to  be  infected.  It  has  also  been  noted  as  occurring  in  the  Philippine 
Islands.  A  few  cases  have  been  observed  in  this  country.  The  disease 
also  has  been  encountered  in  the  tiger,  dog,  cat,  and  in  swine. 

The  exciting  cause  of  pulmonary  distomatosis  is  a  trcmatode  worm, 
the  lung  fluke,  known  as  Paragonimus  W  ester  mannii .  The  worm  is 
almond-shaped  and  in  the  fresh  state  of  a  pinkish  or  reddish-brown 
color.  The  eggs  are  golden  yellow  in  color  and  larger  than  the  eggs  of 
other  parasites  common  to  man.  They  may  be  seen  with  the  unaided 
eye  as  brownish  specks  if  a  small  portion  of  sputum  containing  them  is 
pressed  between  a  cover  slip  and  slide  and  held  up  t<>  the  light. 


488         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

The  life  history  of  the  first  and  final  stages  only  is  known.  Manson 
found  that  if  the  sputum  containing  the  eggs  is  mixed  with  water  and  the 
water  changed  occasionally,  after  some  weeks,  more  or  fewer  according 
to  temperature,  a  ciliated  embryo  will  develop  in  each  egg.  In  a  short 
time  the  embryo  emerges  from  the  egg  and  swims  about  vigorously  for 
some  hours.  It  thus  seems  probable  that  the  sputum  cast  on  the  ground 
is  washed  down  by  the  rain  or  otherwise  and  so  gets  into  wells  or  pools 
of  water.  Beyond  this  we  have  no  positive  knowledge  but  Manson 
assumes  that  the  embryo  gets  into  a  small  mollusc,  in  which  it  undergoes 
the  evolutionary  changes  characteristic  of  other  distomes.  When  these 
are  completed  it  is  carried  in  the  water  or  by  some  water  plant,  back  to 
man  again. 

Nakagawa1  has  found  encysted  larvae  in  fresh-water  crabs.  The 
encysted  larvae  were  fed  to  puppies.  Examination  after  death  revealed 
a  number  of  cysts  in  the  lungs.  Further  study  showed  that  the  encysted 
larvae  after  they  have  been  taken  into  the  alimentary  tract  of  the  host 
escape  from  the  cysts,  penetrate  the  intestinal  wall  near  the  jejunum  and 
escape  into  the  abdominal  cavity.  They  then  pass  through  the  dia- 
phragm into  the  thoracic  cavity,  scatter  over  the  pleura  and  finally  gain 
entrance  into  the  pulmonary  tissues.  Having  entered  the  parenchyma 
of  the  lung  a  cyst  is  formed  and  the  worm  becomes  full-grown.  Although 
the  parasites  may  become  fixed  in  organs  other  than  the  lungs  the  latter 
seem  to  be  the  most  favorable  place  for  their  development. 

Morbid  Anatomy. — The  lungs  of  individuals  who  have  become  the 
victims  of  this  parasite  contain  a  varying  number  of  cysts  or  burrows 
which  harbor  the  worm.  These  cysts  are  commonly  about  the  size  of  a 
hazelnut  but  they  may  be  as  large  or  even  larger  than  a  walnut.  They 
may  be  located  at  any  point  within  the  parenchyma  of  the  lung  but  are 
most  frequently  found  toward  the  periphery  of  the  organ.  If  located 
just  beneath  the  pleura  they  may  project  as  hemispherical  nodules  of 
a  bluish-gray  color.  The  frequency  with  which  the  cysts  occur  near  the 
periphery  of  the  lungs  leads  to  secondary  inflammation  of  the  pleura  and 
as  a  result  adhesions  are  common. 

According  to  Manson  these  so-called  burrows  are  little  tumors  or 
thickenings  produced  by  inflammatory  exudate  in  the  parenchyma  of  the 
lung  and  are  riddled  with  small  passages  or  burrows  in  which  the  parasites 
lie.  Each  cyst  or  burrow  contains  one  or  more  worms  and  in  addition 
a  reddish,  dirty  brown,  mucosanguineous  material.  The  cavities  com- 
municate with  the  bronchi  by  one  or  more  passages  and  at  times  neigh- 
boring cysts  communicate  with  each  other  by  tortuous  channels.  Again 
adjacent  cysts  may  rupture  into  each  other  forming  large  irregular 
cavities. 

Although  there  is  a  direct  passage  from  the  burrow  containing  the 
worm  to  the  outside  by  way  of  the  bronchi,  the  worms  themselves  are 
rarely  coughed  up.  According  to  the  size  and  number  of  the  cysts,  a 
certain  amount  of  the  rusty,  ova-bearing  sputum  is  expectorated  or 
swallowed.  The  extent  of  the  infection  has  a  bearing  on  the  severity 
of  the  symptoms.  It  may  be  so  slight  that  the  patient  experiences  no 
difficulty  other  than  the  expectoration  of  a  little  rusty  colored  sputum ; 
on  the  other  hand,  the  patient  may  be  subject  to  recurring  attacks  of 
profuse  hemoptysis. 

1  Jour.  Infect.  Dis.,  xvii,  No.  2,  p.  131.1 


DISEASES    OF    THE    LUNGS  489 

While  the  lung  is  the  normal  habitat  of  the  parasite,  it  may  be 
found  in  other  parts  of  the  body  such  as  the  scrotum,  liver,  peritoneum, 
diaphragm,  lymph  nodes,  and  especially  the  brain.  In  the  latter  situa- 
tion it  may  produce  the  symptoms  of  Jacksonian  epilepsy  or  brain 
tumor.  Japanese  observers  have  reported  instances  of  brain  infection 
in  which  cysts  containing  both  the  ova  and  worms  occurred. 

Symptoms. — The  disease  is  usually  insidious  in  its  onset  and  as 
ordinarily  seen,  not  attended  with  marked  constitutional  symptoms  or 
by  emaciation.  The  distinctive  features  of  pulmonary  distomatosis 
are  cough,  which  is  usually  worse  on  arising  in  the  morning,  the  expectora- 
tion of  rusty,  brown  or  dark  red  sputum  and  the  occurrence  of  recurring 
attacks  of  hemoptysis.  Owing  to  the  close  proximity  of  the  "burrows" 
to  the  visceral  layer  of  the  pleura,  inflammatory  changes  in  the  latter 
are  common,  thus  giving  rise  to  varying  degrees  of  chest  pain.  In  com- 
mon with  other  chronic  pulmonary  lesions  patients  who  are  subject  to 
this  infection  are  apt  to  suffer  from  dyspnea,  and  mild  asthmatic  attacks. 
If  the  attacks  of  hemoptysis  are  frequent,  the  patient  may  become  anemic 
and  in  such  cases  functional  murmurs  are  heard.  As  a  rule  there  is  no 
fever.  The  severity  of  the  symptoms  depend  largely  on  the  amount  of 
the  pulmonary  damage.  The  disease  may  be  so  limited  in  extent  as  to 
cause  no  inconvenience  other  than  the  slight  cough  and  expectoration. 
In  other  instances,  the  patient  is  subject  to  frequent  attacks  of  profuse 
bleeding  and  a  gradual  deterioration  in  health. 

In  the  great  majority  of  instances  the  lungs  alone  are  involved,  but 
as  already  pointed  out,  other  portions  of  the  body  may  be  involved 
either  primarily  or  as  a  complication  of  the  pulmonary  infection.  Next 
to  the  lungs  the  brain  seems  to  be  the  most  vulnerable  point.  Involve- 
ment of  the  brain  gives  rise  to  a  variety  of  nervous  symptoms:  epilepsy, 
hemiplegia,  paresis  of  the  extremities,  headache,  vertigo,  etc. 

Physical  Signs. — In  common  with  other  pulmonary  infections  which 
simulate  tuberculosis  there  is  nothing  distinctive  in  the  physical  signs 
which  will  serve  to  differentiate  the  two  conditions.  Physical  signs  may 
be  entirely  wanting  if  the  lesion  is  small  or  deep-seated.  In  cases  with 
extensive  involvement  of  the  pleura  there  may  be  marked  retraction  of 
the  chest  wall  and  a  very  limited  respiratory  movement.  The  lesion 
may  be  single  and  circumscribed  or  there  may  be  a  number  of  such  areas 
over  which  the  percussion  note  is  impaired  and  the  breath  sound  sup- 
pressed or  broncho-vesicular  in  character.  Rales  may  be  present  also. 
Signs  of  cavity  formation  are  not  commonly  encountered. 

Diagnosis. — Inasmuch  as  cough,  blood-streaked  sputum  or  a  frank 
hemoptysis  and  chest  pain  are  the  principal  symptoms  of  pulmonary 
distomatosis,  the  disease  must  be  distinguished  from  other  conditions 
in  which  the  same  symptoms  occur.  It  is  evident  that  the  disease  which 
most  commonly  gives  rise  to  such  symptoms  is  tuberculosis.  So  far  as 
the  symptoms  are  concerned  no  distinction  between  the  two  is  possible 
and  if  the  lung  fluke  is  located  in  the  pulmonary  apices  the  confusion  is 
increased.  A  very  important  point  is  the  question  of  whether  the  individ- 
ual has  lived  in  the  endemic  zone.  The  diagnosis  must  rest  on  the 
microscopic  examination  of  the  sputum  and  this  is  easily  made  from  the 
presence  of  the  eggs  and  the  absence  of  tubercle  bacilli.  Both  tuber- 
culosis and  distomatosis  may  occur  in  the  same  individual.  In  suspected 
cases  in  which  it  is  impossible  to  obtain  the  sputum  the  stools  should  be 


490         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

examined  for  the  ova.  It  is  said  that  the  presence  of  Charcot-Leyden 
crystals  in  the  sputum  is  strongly  suggestive  of  distomatosis  in  those 
living  in  infected  regions  and  should  lead  to  a  careful  search  for  the  eggs. 

Syphilis  of  the  Respiratory  Tract 
larynx 

Syphilis  may  attack  the  larynx  both  as  an  early  and  a  late  manifesta- 
tion of  the  disease  but  is  far  more  common  in  the  so-called  secondary 
stage.  Indeed  a  very  large  proportion  of  individuals  suffering  from 
acquired  syphilis  manifest  symptoms  of  laryngeal  trouble,  usually,  how- 
ever, of  a  transient  nature.  Any  portion  of  the  larynx  may  be  involved 
— the  epiglottis,  the  vocal  cords  or  the  body  of  the  larynx. 

Examination  of  the  larynx  during  the  active  stage  of  syphilis  will 
often  show  the  presence  of  catarrhal  changes,  congestion  of  the  mucous 
membrane,  mucous  patches  or  slight  erosions.  The  catarrhal  inflamma- 
tion or  congestion  often  becomes  apparent  at  the  time  the  cutaneous 
eruption  first  makes  its  appearance.  In  other  instances  the  laryngeal 
lesion  develops  later.  Mucous  patches  are  much  less  common.  They 
may  form  superficial  erosions  or  in  severe  cases  an  ulcer  may  be  formed. 
Edema  of  the  laryngeal  tissues  may  accompany  any  of  these  changes. 
Unless  the  individual  is  cured  there  is  a  tendency  for  the  laryngeal  lesions 
to  recur. 

Tertiary  lesions  of  the  larynx  are  relatively  rare  and  usually  appear 
very  late.  A  gumma  varying  in  size  from  a  pinhead  to  a  hazelnut,  is 
usually  the  first  manifestation.  The  gumma  may  break  down  forming  a 
deep  ulcer  which  in  the  process  of  healing  may  produce  serious  deformi- 
ties as  the  result  of  retraction  of  the  scar  tissue.  Partial  or  even  com- 
plete laryngeal  stenosis  may  be  produced.  In  other  instances  the  ter- 
tiary disease  attacks  the  cartilaginous  portion  of  the  larynx.  The 
disease  may  extend  and  by  invading  the  tissues  about  the  larynx  produce 
an  external  fistula. 

Sy miners1  in  a  study  of  4880  autopsy  protocols  found  the  anatomic 
confirmation  of  the  existence  of  syphilis  in  314  cases,  or  6.5  per  cent.  The 
larynx  was  involved  in  12.  In  5  there  were  cicatricial  lesions;  in  5 
ulcerative  lesions,  in  1  a  gumma  and  in  1  a  leukoplacia  of  the  epiglottis. 
In  addition  there  were  17  cases  in  which  the  epiglottis  was  deformed  in 
association  with  syphilitic  changes  at  the  base  of  the  tongue. 

In  the  secondary  stage  the  most  constant,  and  often  the  only  symp- 
tom, is  hoarseness.  A  cough  is  more  often  absent  than  present.  Com- 
plete aphonia  sometimes  occurs.  Rarely  marked  difficulty  in  breathing 
occurs  as  the  result  of  edema  of  the  larynx. 

In  the  tertiary  stage  the  trouble  usually  first  manifests  itself  by 
hoarseness  which  may  develop  into  complete  loss  of  the  voice.  If 
cicatricial  changes  occur,  the  difficulty  in  breathing  becomes  progressively 
worse.  Sudden  closure  of  the  laryngeal  opening  may  occur.  The 
difficulty  in  breathing  is  both  inspiratory  and  expiratory  and  is  ac- 
companied by  more  or  less  stridor.  If  the  ulcerative  process  involves 
the  epiglottis  or  the  arytenoids  the  patient  may  experience  pain  on 
swallowing. 

1  Jour.  Am.  Med.  Assoc,  May  6,  1916. 


DISEASES    OF   THE    LUNGS  491 

TRACHEA  AND  BRONCHI 

Morbid  Anatomy. — Involvement  of  the  trachea  alone  is  rare.  In 
1903,  Conner1  collected  128  cases  of  syphilis  of  the  trachea  and  bronchi. 
Symmers2  found  4  instances,  among  4880  autopsies,  in  which  the  lesion 
was  limited  to  the  trachea;  and  Lord3  states  that  2  instances  of  syphilitic 
ulceration  of  the  trachea  were  found  among  3000  autopsies  at  the  Massa- 
chusetts General  Hospital. 

Lesions  in  the  trachea  are  present,  as  a  rule,  in  the  upper  or  lower 
third,  especially  at  the  bifurcation.  Involvement  of  the  lower  portion 
of  the  trachea  and  the  main  bronchi  is  not  uncommon.  One  or  both  of 
the  primary  divisions  of  the  bronchi  may  be  involved. 

The  tertiary  lesions  of  the  trachea  and  bronchi  are  practically  always 
late  manifestations  and  may  be  due  to  hereditary  as  well  as  the  acquired 
form  of  the  disease. 

The  mucous  membranes  of  the  trachea  and  large  bronchi  may  be  the 
seat  of  catarrhal  change  during  the  secondary  stage.  This  change  may 
be  the  result  of  an  increased  susceptibility  to  "colds"  during  the  acute 
stage  of  syphilis  or,  as  in  the  case  of  the  larynx,  to  the  presence  of  mucous 
patches. 

As  a  tertiary  manifestation  syphilis  may  occur  in  the  trachea  or  large 
bronchi  as  a  gummatous  infiltration.  At  first  this  causes  considerable 
swelling.  The  gumma  may  become  absorbed  leaving  as  evidence  of  its 
presence  a  scar  or  it  may  break  down  and  produce  an  ulcer  and  this 
in  turn  may  heal  and  become  a  scar.  A  syphilitic  ulcer  in  the  lower  por- 
tion of  the  trachea  or  in  one  of  the  primary  bronchi  may  perforate  or 
extend  into  the  surrounding  mediastinal  tissues,  the  esophagus  or  the 
pulmonary  artery.  Occasionally  the  cartilaginous  structures  become 
necrosed  and  either  may  be  entirely  absorbed  or  small  pieces  of  cartilage 
may  slough  off  and  be  expectorated. 

When  healing  follows  either  a  gumma  or  an  ulcer,  the  resulting  scar 
tissue  usually  contracts  and  often  produces  marked  deformity  or  even 
complete  stenosis.  At  the  point  of  the  scar  the  lumen  is  narrowed  by  an 
annular  or  membranous  stricture  or  strictures.  Dilatation  of  the  trachea 
or  bronchi  may  occur  above  and  below  the  constricted  point. 

Symptoms. — During  the  secondary  stage  of  syphilis  involvement  of 
the  trachea  may  manifest  itself  as  a  simple  trachitis.  There  is  cough, 
expectoration  and  some  substernal  soreness. 

As  a  late  manifestation  the  first  evidence  of  trouble  is  usually  a  cough, 
which  at  first  is  dry  and  unproductive;  later  it  is  accompanied  by  mucoid 
or  mucopurulent  sputum.  If  the  disease  occurs  in  the  form  of  a  gumma 
which  becomes  absorbed,  the  symptoms  rarely  consist  of  anything  more 
than  a  cough  with  or  without  the  presence  of  sputum.  If,  however,  an 
ulcer  forms  the  sputum  is  often  blood-streaked  and  a  frank  hemoptysis 
is  not  unusual.  A  few  instances  have  been  recorded  in  which  a  fatal 
hemorrhage  followed  perforation  of  an  ulcer  into  the  pulmonary  artery. 
Substernal  pain  may  occur  and  in  some  instances  there  is  also  dysphagia. 

With  the  formation  of  a  stricture  the  symptoms  of  stenosis  are  added 
to  the  picture.     As  soon  as  the  stricture  begins  to  offer  obstruction  to  the 

1  Am.  Jour.  Med.  Sc,  vol.  cxxvi,  p.  57. 

2  hoc.  cil. 

3  "Diseases  of  the  Bronchi,  Lungs  and  Pleura,"  1915. 


492  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

ingress  and  the  egress  of  the  air,  the  patient  begins  to  suffer  from  dyspnea 
which  is  more  or  less  marked,  depending  on  the  degree  of  the  stenosis. 
The  dyspnea  may  be  persistent  or  it  may  occur  in  paroxysms.  Suffo- 
cative attacks  may  come  on  very  suddenly;  sometimes  without  apparent 
cause,  in  other  instances  as  the  result  of  sudden  exertion.  The  diffi- 
culty in  breathing  is  both  inspiratory  and  expiratory  and  is  usually 
attended  by  marked  stridor.  During  the  attack  the  patient  becomes 
cyanosed,  the  pulse  becomes  weak  and  there  may  be  unconsciousness. 

Physical  Signs. — The  respiratory  movements  of  the  chest  are  dimin- 
ished, the  breath  sounds  are  feeble  and  the  tissues  at  the  root  of  the  neck, 
the  lower  intercostal  spaces  and  the  epigastrium  show  inspiratory 
retraction.  Rarely  one  of  the  main  bronchi  may  be  stenosed.  This  is 
to  be  suspected  if  there  is  unilateral  diminution  of  the  respiratory  incur- 
sion and  suppression  of  the  auscultatory  phenomena.  There  may  be 
present  also,  over  the  site  of  the  stricture,  a  whistling  quality  of  the 
respiratory  sounds. 

In  Conner's1  series  death  occurred  in  eleven  instances  during  a 
suffocative  attack. 

Diagnosis. — Prior  to  the  formation  of  a  stricture  tuberculosis  is  most 
apt  to  be  the  diagnosis  owing  to  the  cough,  mucopurulent  sputum  and 
the  appearance  of  blood.  The  persistent  absence  of  tubercle  bacilli  and 
of  abnormal  physical  signs  in  the  lungs  renders  the  correctness  of  such  a 
diagnosis  doubtful.  Syphilis  is  always  to  be  thought  of,  especially  if 
there  is  a  history  of  that  disease,  the  presence  of  syphilitic  stigmata 
elsewhere  and  the  presence  of  a  positive  Wassermann  test. 

If  stenosis  has  taken  place  the  obstruction  may  be  due  to  a  syphilitic 
stricture,  to  a  foreign  body  or  to  the  presence  of  a  tumor,  aneurism  or 
enlarged  lymph  node.  The  X-rays  and  the  use  of  the  bronchoscope 
should  always  be  employed  in  such  cases. 

The  Lungs 

Syphilis 'of  the  lungs  has  always  been  looked  upon  as  a  rare  condi- 
tion. The  diagnosis  is  not  often  made  during  life.  If  the  lesions  have 
become  healed  the  resulting  scar  tissue  differs  in  no  particular  from  that 
produced  by  a  non-specific  inflammation,  hence,  it  is  difficult  to  prove, 
even  after  death,  whether  syphilis  has  been  present  or  not. 

It  is  quite  likely  that  pulmonary  syphilis  will  become  less  of  a  rarity 
now  that  we  know  the  exciting  cause.  Clinically  the  most  important 
addition  to  our  knowledge  has  been  the  introduction  of  the  Wassermann 
test. 

Morbid  Anatomy. — The  incidence  of  pulmonary  syphilis  is  based 
entirely  on  the  finding  of  the  lesions  in  the  lung  which  are  unmistakably 
luetic  in  character.  As  already  stated,  extensive  fibrosis  of  the  lung  or 
the  presence  of  localized  areas  of  scar  tissue  may  or  may  not  be  syphilitic; 
as  a  rule  such  lesions  are  rarely  classed  as  such.  Warthin2  has  reported 
recently  a  histological  study  of  the  pancreas  in  individuals  who  had  had 
syphilis.  He  was  able  to  demonstrate  that  the  pancreas  showed  un- 
mistakable evidences  of  the  presence  of  areas,  of  various  sizes,  which 
were  due  to  syphilitic  changes.     In  many  instances  the  presence   of 

1  hoc  tit. 

-  Trans.  Assoc.  Am.  Phys.,  1916. 


DISEASES    OF    THE    LUNGS  493 

spirochetes  could  be  demonstrated  also.  It  is  quite  possible  that  if 
the  lungs  are  subjected  to  a  similar  study  syphilis  will  be  found  to  be 
a  more  frequent  invader  than,  at  present,  is  believed  to  be  the  case. 

Based  on  present  standards,  syphilis  of  the  lungs  in  adults  is  a  rare 
condition.  This  is  shown  by  the  following  figures:  Fowler  was  able 
to  find  but  12  examples  of  the  disease,  2  of  which  were  doubtful,  in  the 
museums  of  the  London  hospitals.  Among  2800  autopsies  at  the  Johns 
Hopkins  Hospital  there  were  12  cases  with  syphilitic  disease  of  the  lungs 
and  8  of  these  were  due  to  the  congenital  form  (Osier);- among  3000 
autopsies  at  the  Massachusetts  General  Hospital  but  1  case  showing 
indurative  pneumonia,  with  cavity  formation,  was  found  (Lord) ;  in  a 
study  of  4880  autopsy  protocols,  314  of  which  showed  lesions  due  to 
syphilis,  Symmers1  found  the  lungs  involved  in  12  cases  and  the  presence 
of  syphilitic  pleural  scars  in  2  more. 

Congenital  Syphilis. — The  only  type  of  pulmonary  syphilis  about 
which  there  is  a  general  agreement  is  that  seen  in  new-born  syphilitic 
children.  In  this  form  of  the  disease  gummata  may  occur,  but  as  a  rule 
are  rarely  seen.  The  typical  lesion  is  that  known  as  white  pneumonia. 
The  lung  of  a  syphilitic  fetus  or  infant  is  much  increased  in  size  and  may 
be  marked  by  the  ribs.  It  presents  on  section  a  dry,  smooth  surface, 
grayish  or  yellowish- white  color,  resembling  very  closely  the  cut  surface 
of  the  pancreas.  The  areas  of  consolidation  may  occur  in  scattered 
patches  throughout  both  lungs  or  they  involve  an  entire  lobe. 

The  chief  changes  are  cellular  infiltration  involving  the  alveolar 
walls  and  proliferation  of  the  interlobular  connective  tissue  thus  giving 
rise  to  an  interstitial  pneumonia.  Stained  sections  from  the  lungs  of 
syphilitic  children  show  an  enormous  number  of  the  spirochatae  of 
syphilis. 

For  the  most  part  this  type  of  pulmonary  syphilis  is  of  pathological 
interest  only. 

Acquired  Syphilis. — In  acquired  syphilis  three  types  of  the  disease 
are  encountered  in  the  lung,  namely,  gummata,  fibroid  changes  and  areas 
of  consolidation  and  catarrh. 

1.  Gummata. — When  the  disease  occurs  in  the  lungs  in  this  form  the 
gummata  are  apt  to  be  quite  numerous.  They  vary  greatly  in  size 
ranging  from  that  of  a  millet  seed  to  a  hen's  egg.  In  the  early  stages  of 
their  development  gummata  are  grayish  red  or  grayish  white  in  color, 
somewhat  translucent,  and  are  surrounded  by  an  area  of  congestion. 
Later  they  become  opaque  and  somewhat  caseous.  In  addition  they 
become  walled  off  by  a  thick  fibrous  envelope.  Occasionally  a  gumma 
may  caseate  and  empty  into  a  bronchus,  thus  producing  a  pulmonary 
cavity.  This  is  a  very  rare  manifestation  of  the  disease  known  as  syphi- 
litic phthisis.  Eventually  the  gummata  may  become  entirely  healed, 
leaving  behind  them  nothing  but  a  tough  mass  of  puckered  scar  tissue 
which  cannot  be  distinguished  from  similar  scars  produced  by  tubercles 
or  an  abscess. 

The  gummata  may  occur  in  any  portion  of  lung  but  are  usually  to  be 
found  about  the  hilus  and  in  the  lower  lobes. 

2.  Fibroid  Induration. — This  is  a  much  more  frequent  manifestation 
than  the  formation  of  gummata  although  the  latter  may  also  occur  in 
association  with  the  fibroid  changes.     Now  that  the  exciting  cause  of 

1  hoc.  cit. 


494         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

syphilis  is  known  the  presclerotic  changes  are  better  understood.  Fol- 
lowing the  lodgment  of  spirochatse  in  the  lung  an  inflammatory  reac- 
tion sets  in.  This  takes  the  form  of  an  extensive  cellular  infiltration 
together  with  an  overgrowth  of  the  connective  tissue  in  the  interlobular 
septa  and  proliferation  and  desquamation  of  the  alveolar  epithelium. 
The  alveolar  walls  become  greatly  thickened  as  do  also  the  blood-vessels. 
Gradually  the  entire  area  is  converted  into  dense  fibrous  tissue.  When 
this  stage  is  reached,  the  clinical  picture  is  that  of  pulmonary  fibrosis  or 
bronchiectasis.  How  frequently  syphilis  is  the  exciting  cause  of  a 
diffuse  pulmonary  fibrosis  is  problematical. 

The  indurative  changes  may  originate  at  the  hilus  of  the  lung  and 
extend  outward  along  the  bronchi  and  blood-vessels  or  the  starting  point 
may  be  the  pleura  and  inlobar  septa.  The  process  is  usually  unilateral 
and  at  most  involves  only  a  portion  of  one  lobe;  if  several  lobes  are  im- 
plicated, it  is  the  portions  which  adjoin  the  root  of  the  lung. 

3.  Consolidation  and  Catarrh. — In  addition  to  the  types  just  mentioned 
a  focal  form  is  described  in  which  the  lesion  consists  of  an  area  of  consoli- 
dation and  catarrh.  It  may  be  situated  around  the  root  of  the  lung  or  it 
may  occur  at  one  apex.  The  general  opinion  has  been  that  the  apices 
are  rarely  involved,  but  it  would  be  rather  surprising,  in  view  of  the 
wonderfully  diverse  forms  in  which  the  localization  of  syphilis  mani- 
fests itself,  if  the  upper  portions  of  the  lung  should  escape.  Lewis  and 
I1  have  reported,  from  the  Phipps  Institute,  six  cases  in  which  the  physi- 
cal signs  pointed  to  a  focal  lesion  in  the  apex  and  in  which  the  evidence 
seemed  to  be  conclusive  that  a  latent  syphilitic  process  was  present. 

In  the  secondary  stage  of  syphilis  symptoms  and  physical  signs 
pointing  to  a  catarrhal  condition  of  one  apex  are  occasionally  encountered. 
Dunham2  has  referred  to  several  cases  of  this  nature.  He  believes  the 
changes  are  analogous  to  those  occurring  in  the  larynx  and  trachea 
during  the  secondary  stage. 

Symptoms. — The  symptoms  which  have  been  noted  as  occurring  in 
individuals  suffering  from  syphilitic  invasion  of  the  lungs  are  not  distinc- 
tive. They  are  such  as  may  occur  in  any  inflammatory  process  which 
involves  the  pulmonary  tissues.  In  addition  the  symptoms  will  vary 
accordingly  as  the  patient  is  seen  in  the  active  stage  of  the  process  or 
during  the  stage  when  chronic  fibroid  changes  have  developed. 

The  following  pulmonary  symptoms  are  usually  present:  Cough, 
which  may  be  dry  and  unproductive  or  accompanied  by  a  moderate 
amount  of  expectoration  which  is  yellowish  or  greenish  in  color.  Hemop- 
tysis is  not  common  although  in  one  case  which  I  had  under  observation 
there  were  frequent  attacks  of  blood  spitting.  Dyspnea  is  often  present 
and  may  be  very  marked  in  those  cases  in  which  there  are  extensive 
fibroid  changes.  In  some  instances  it  is  asthmatic  in  character.  Hoarse- 
ness may  be  a  prominent  symptom  as  the  result  of  changes  in  the  larynx. 

If  the  case  is  seen  after  the  fibroid  induration  has  existed  for  some 
time  the  clinical  picture  is  that  of  cirrhosis  of  the  lung  with  or  without 
dilatation  of  the  bronchi. 

Some  years  ago  E.  G.  Janeway3  emphasized  the  fact  that  when  the 
viscera  become  involved  during  the  tertiary  stage  of  the  disease,  a  moder- 

1  Am.  Jour.  Med.  Sc,  August,  1915. 

2  Kelly's  Stereo  Clinic,  Section  xxxvii. 

3  Trans.  Assoc.  Am.  Phys.,  1898. 


DISEASES    OF   THE    LUNGS  495 

ate  amount  of  fever  is  usually  present,  emaciation  is  marked  and  night 
sweats  are  of  frequent  occurrence.  These  symptoms  are  often  associated 
with  pain  in  the  right  side  due  to  a  syphilitic  perihepatitis.  Further- 
more, one  is  apt  to  find,  on  careful  examination,  some  other  noticeable 
evidence  of  syphilis,  such  as  an  indurated  testicle  or  enlargement  and 
tenderness  of  the  ribs  or  clavicles  at  the  sternal  attachments. 

Warthin1  has  shown  that  next  to  the  aorta  and  heart  the  testes  are 
the  most  frequent  sites  of  a  syphilitic  infection.  In  a  pathological  study 
of  36  cases  of  syphilis  occurring  in  males,  the  majority  of  which  were 
latent  and  unrecognized  during  life,  an  orchitis  fibrosa  was  present  in  31. 
Among  171  male  subjects  of  late  acquired  syphilis  Symmers2  found  a 
chronic  interstitial  orchitis  in  67  or  39  per  cent.  He  believes  that  the 
diminished  size  of  the  testicle  and  its  increased  consistency  furnish 
valuable  evidence  both  in  the  clinical  and  anatomical  diagnosis  of 
syphilis. 

In  the  case  of  women  a  history  of  miscarriages  is  extremely  significant. 

Physical  Signs. — If  the  syphilitic  manifestation  is  limited  to  the 
larynx,  trachea  or  main  bronchi,  the  diagnosis  is  a  matter  of  direct  inspec- 
tion by  means  of  the  laryngoscope  or  bronchoscope.  Unless  the  examiner 
has  had  special  training  in  this  work  the  case  should  be  referred  for  an 
expert  opinion.  Involvement  of  the  smaller  bronchi  or  parenchyma 
of  the  lung  does  not  produce  physical  signs,  which  are  indicative  of 
syphilis.  In  the  vast  majority  of  cases  the  primary  diagnosis  is  that  of 
tuberculosis,  either  incipient  or  advanced,  depending  on  whether  there  is 
a  focal  lesion,  or  a  diffuse  fibroid  process.  The  former  may  occur  about 
the  root  of  the  lung,  or  at  the  apices.  When  an  apex  is  affected  the  signs 
differ  in  no  particular  from  those  encountered  in  incipient  tuberculosis. 
In  the  fibroid  form  the  condition  is  usually  mistaken  for  fibroid  phthisis 
or  bronchiectasis.  In  very  rare  instances  pulmonary  gummata  may 
break  down  and  empty  into  a  bronchus,  thus  forming  a  cavity.  In 
such  instances  the  physical  signs  would  be  identical  with  those  encoun- 
tered in  tuberculosis. 

The  diagnosis  of  syphilis  of  the  lung  is  almost  invariably  made  by  a 
process  of  exclusion.  An  individual  who  has  complained  of  cough,  with 
or  without  expectoration,  for  several  months,  who  has  slight  fever  and 
malaise  and  has  suffered  from  some  loss  of  weight,  is  almost  certain  to 
be  regarded  as  being  tuberculous.  Pulmonary  signs  may  be  wanting  or 
may  be  present  at  one  or  the  other  apex.  If  the  physical  signs  are  located 
at  the  base  or  root  of  the  lung  one's  suspicions  should  be  aroused.  As  a 
general  rule  the  true  nature  of  the  trouble  escapes  detection  and  is  recog- 
nized only  when  the  patient  fails  to  improve  or  there  develops  some  other 
evidence  of  the  disease  such  as  an  orchitis  or  bone  lesion.  Now  that  the 
Wassermann  test  is  available  it  should  always  be  applied  in  suspicious 
cases.  The  therapeutic  test  is  also  of  service  in  determining  the  true 
nature  of  the  trouble.  Following  the  use  of  salvarsan  or  mixed  treatment 
the  physical  signs  and  symptoms  show  decided  improvement.  Inas- 
much as  iodide  of  potassium  has  a  marked  tendency  to  cause  a$breaking 
down  of  tuberculous  lesions  in  the  lung,  the  drug  should  never  be  admin- 
istered until  every  means  has  been  employed  to  exclude  tuberculosis. 

The  following  cases  will  serve  to  indicate  the  various  manifestations 
of  pulmonary  syphilis: 

lLoc.  tit.,  1914.  2Loc.  cit. 


496         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Case  I  (Phipps  Institute  Xo.  9485). — Female,  aged  28,  first  came  to  the  Phipps 
Institute  June  10,  1911.  She  gave  a  history  of  having  had  repeated  attacks  of  blood 
spitting  for  five  years.  Her  first  pregnancy  resulted  in  a  miscarriage.  During  the 
past  year  she  had  had  a  cough,  considerable  greenish  expectoration,  night  sweats  and 
had  lost  during  the  past  two  years  30  pounds.  She  also  complained  of  pain  over  the 
base  of  the  right  lung  (perihepatitis).  There  was  a  slight  elevation  of  temperature, 
99°  to  100°F.  Examination  of  right  lung  showed  some  flattening  beneath  right 
clavicle,  diminished  expansion,  impairment  of  the  percussion  note  and  broncho- 
vesicular  breathing.  She  was  sent  to  a  sanatorium  and  remained  away  several 
months.  Although  she  gained  16  pounds  in  weight,  the  pulmonary  symptoms  re- 
mained unchanged. 

On  her  return  to  the  Institute  her  sputum  was  repeatedly  examined  for  tubercle 
bacilli  as  well  as  other  organisms  but  was  always  found  to  be  negative.  The  Wasser- 
mann  test  was  strongly  positive.  On  April  27,  1912,  was  given  salvarsan  and  after- 
wards put  on  mixed  treatment.  Three  Wassermann  tests  within  the  next  six  months 
were  negative.  Guinea  pigs  inoculated  with  her  sputum  were  killed  and  found  to  be 
free  from  tuberculosis.  The  pulmonary  symptoms  steadily  improved.  During  the 
past  year  she  became  pregnant  and  recently  was  confined.  At  the  present  time, 
February  1,  1916,  she  weighs  188  pounds  and  is  apparently  well  in  every  way. 

Case  II  (Phipps  Institute,  Xo.  13391). — Female,  aged  34  years,  first  visited  the 
Phipps  Institute  August  20,  1914.  Her  family  history  was  negative.  She  had  been 
married  eleven  years  and  had  had  three  miscarriages.  Xo  living  children.  There 
was  no  history  of  an  initial  lesion  nor  of  secondaries.  She  came  to  the  dispensary 
because  of  a  cough,  greenish-colored  expectoration,  night  sweats  and  some  loss  in 
weight.  In  addition  she  complained  of  precordial  pain,  which  hadjbeen  present 
intermittently  for  six  years.  For  four  years  she  had  suffered  from  attacks  of  burning 
and  tingling  in  the  legs. 

Examination. — Some  flattening  beneath  the  right  clavicle,  impairment  of  the 
percussion  note,  and  broncho-vesicular  breathing.  Heart  was  negative.  The  reflexes 
were  exaggerated. 

During  the  first  six  months  she  was  under  observation  the  night  sweats,  morning 
cough,  and  expectoration  persisted,  and  the  sputum  was  blood-tinged  on  one  occasion. 
There  was  also  a  slight  rise  in  temperature.  The  sputum  was  negative  for  tubercle 
bacilli.  In  February,  1915,  she  first  complained  of  nocturnal  headache.  This 
gradually  became  worse,  and  finally  was  so  severe  as  to  interfere  with  her  sleep.  The 
Wassermann  test  was  strongly  positive.  Under  mixed  treatment  the  headache  was 
relieved.  Later,  following  the  administration  of  salvarsan,  the  cough  ceased  and  the 
amount  of  expectoration  was  greatly  reduced. 

Case  III. — A  male  aged  30  was  admitted  to  the  White  Haven  Sanatorium  several 
years  ago  with  a  history  of  having  been  ill  for  some  months.  He  had  lost  about  25 
pounds,  had  a  cough,  expectoration,  slight  fever  and  marked  hoarseness.  Examina- 
tion of  the  lungs  showed  impairment,  feeble  breath  sounds  and  a  few  fine  rales  at  the 
left  apex.  The  case  seemed  to  be  clearly  one  of  pulmonary  and  laryngeal  tuber- 
culosis. Two  weeks  after  his  admission  the  trouble  in  his  larynx  was  found  to  be 
specific  in  nature.  Under  mixed  treatment  he  made  a  complete  recovery,  the  pul- 
monary signs  entirely  disappearing. 

Several  cases  have  been  sent  to  White  Haven  because  of  marked 
hoarseness  which  on  examination  proved  to  be  syphilitic  in  origin.  With 
the  exception  of  case  just  mentioned  pulmonary  signs  were  wanting. 
These  cases  serve  to  emphasize  the  necessity  of  a  competent  laryngological 
examination,  as  delay  in  instituting  antisyphilitic  treatment  may  lead  to 
serious  and  permanent  damage  of  the  larynx, 

Case  IV. — -A  middle-aged  woman  began  to  suffer  from  ill  health  about  three 
years  prior  to  coming  under  observation.  She  had  lost  weight,  had  a  persistent  cough 
with  expectoration  and  in  addition  suffered  greatly  from  dyspnea.  At  times  she  had 
moderately  severe  asthmatic  attacks.  Examination  of  her  chest  showed  restriction 
of  motion  at  the  right  base;  the  percussion  note  was  dull,  especially  anteriorly  at  the 
base,  and  the  breath  sounds  were  broncho-vesicular  in  type.  She  had  been  under 
treatment  during  most  of  this  period  for  tuberculosis  but  with  no  improvement. 
Persistent  absence  of  tubercle  bacilli  lead  to  a  Wassermann  test  which  was  positive. 
Several  injections  of  salvarsan  brought  about  some  improvement  in  the  symptoms  but 


DISEASES    OF    THE    LUNGS  497 

the  physical  signs  remained  unchanged.  In  this  case  the  pulmonary  process  had 
probably  advanced  to  permanent  fibrosis. 

Case  V  (Phipps  Institute  Case  No.  1628). — A  female,  aged  52.  Admitted  to  the 
Phipps  Institute  in  1903.  She  gave  a  definite  history  of  having  acquired  syphilis  at 
the  age  of  15.  There  were  present  interstitial  keratitis,  perforation  of  the  palate,  and 
numerous  deep  scars  scattered  over  the  body.  The  present  illness  began  five  years 
prior  to  admission  with  cough  and  pain  in  the  right  side.  Two  j^ears  later  she  had  a 
hemoptysis  and  during  the  three  following  years  had  had  over  30  such  attacks.  On 
admission  she  had  cough,  greenish  expectoration,  night  sweats,  dyspnea  and  some  loss 
in  weight.  The  sputum  has  been  examined  repeatedly  for  tubercle  bacilli,  as  well  as 
other  organisms,  but  always  with  negative  results. 

Examination  of  the  chest  showed  restriction  of  motion  on  right  side,  most  marked 
at  the  base,  dulness  up  to  the  angle  of  the  scapula,  distant  breath  sounds  and  fine 
cracking  rales.  At  the  angle  of  the  scapula  there  was  a  small  area  of  tympany  on 
percussion,  whispering  pectoriloquy  and  bronchial  breathing. 

This  woman  has  been  seen  from  time  to  time  during  the  past  twelve  years.  The 
symptoms,  including  an  occasional  hemoptysis,  have  remained  unchanged.  It  seems 
probable  that  in  this  case  the  pulmonary  process  (gumma  or  diffuse  fibroid  induration) 
has  ended  in  a  fibrosis  of  the  right  lower  lobe  and  that,  in  addition,  the  bronchi  have 
become  dilated.     A  similar  case  has  been  reported  bjr  Osier.1 

Diagnosis. — The  most  frequent  error  is  that  of  mistaking  pulmonary- 
syphilis  for  tuberculosis.  The  symptoms  are  often  identical.  If  the 
physical  signs  are  elicited  about  the  hilus  or  at  the  base  of  the  lung, 
tuberculosis,  almost  invariably,  can  be  ruled  out.  If,  however,  the 
lesion  is  located  in  the  apex  of  the  lung  syphilis  may  simulate  tubercu- 
losis so  closely  as  to  deceive  us  entirely.  To  establish  a  diagnosis  of 
syphilis  the  sputum  must  be  negative  repeatedly  for  tubercle  bacilli, 
or  other  organisms  which  produce  lesions  of  a  similar  nature;  other 
syphilitic  stigmata  must  be  present,  such  as  a  bone  lesion,  keratitis, 
indurated  testicle,  etc.;  and  the  Wassermann  test  must  be  positive.  The 
results  of  antisyphilitic  treatment  also  furnish  valuable  evidence. 
Tuberculosis,  for  instance,  will  not  be  improved  either  by  the  use  of 
salvarsan  or  of  mercury  and  the  iodides.  Syphilis  on  the  other  hand  is 
markedly  improved  or  cured  by  the  use  of  these  drugs  unless  permanent 
fibroid  changes  have  taken  place. 

Syphilis  and  Tuberculosis. — The . prevalence  of  both  these  diseases 
makes  it  inevitable  that  many  cases  are  encountered  in  which  the  same 
individual  is  suffering  from  both  infections. 

In  one  who  has  been  the  victim  of  syphilis  for  many  3rears  the  oc- 
currence of  active  tuberculosis  may  be  brought  about  by  a  lowering  of 
resistance  as  a  result  of  the  primary  infection.  The  course  of  the 
tuberculosis  does  not  differ,  however,  from  that  occurring  in  non-syphilitic 
individuals. 

On  the  other  hand,  if  both  diseases  develop  simultaneously  or  within 
a  short  time  of  each  other,  the  patient  is  apt  to  be  overwhelmed.  The 
tuberculous  infection  is  especially  apt  to  become  extremely  active  and 
to  pursue  a  rapid  and  acute  course.  There  are  exceptions,  of  course, 
but  it  is  generally  recognized  that  the  association  of  the  two  diseases  in 
an  active  form,  is  a  particularly  vicious  one  and  that  the  tuberculosis  is 
rarely  arrested  in  such  cases.  Distressing  examples  of  this  are  often 
seen  in  young  prostitutes  who  have  developed  tuberculosis  in  the  early 
stages  of  the  secondary  period  of  syphilis  and  in  whom  the  tuberculosis 
runs  a  very  rapid  course. 

1  Power  and  Murphy:  "System  of  Syphilis,"  vol.  iii,  p.  24. 
32 


498         DISEASES    OF   THE   BEONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Intrathoracic  Tumors 

For  clinical  purposes  it  is  more  convenient  to  include  all  tumors 
arising  within  the  thorax  under  one  general  heading.  This  seems  best 
because  of  the  fact  that  the  symptoms  to  which  they  give  rise  are  in  the 
majority  of  cases  similar;  although  here  and  there  a  case  is  encountered 
in  which  the  symptoms  and  physical  phenomena  point  definitely  to  the 
growth  being  limited  to  a  bronchus,  the  lung,  the  pleura  or  some  portion 
of  the  mediastinum.  Furthermore,  the  morbid  anatomy  of  the  tumors 
and  the  conditions  under  which  they  invade  the  thoracic  viscera  have  no 
striking  differences. 

Etiology. — The  malignant  tumors  may  be  primary  or  secondary,  the 
latter  being  by  far  the  most  common.  Malignant  growths  may  occur 
at  any  age.  Up  to  the  middle  period  of  life  the  tumor  is  almost  invariably 
sarcomatous  in  nature;  the  younger  the  subject  the  more  certainly  is  this 
■crae.  Beyond  middle  life  the  growth  may  be  a  carcinoma  or  a  sarcoma, 
usually  the  former.  Endotheliomas,  tumors  which  histologically  occupy 
a  position  midway  between  carcinoma  and  sarcoma,  may  occur  at  any 
age.  Primary  malignant  growths  affecting  the  organs  of  the  thorax 
occur  more  frequently  among  males  than  females.  Owing  to  the  greater 
frequency  of  cancer  among  women  metastatic  growths  are  more  frequently 
encountered  in  this  sex.  Trauma  of  the  chest  wall  has  been  cited  as 
an  occasional  cause  of  malignant  disease  arising  within  the  thorax. 

Ancke1  has  reported  the  interesting  fact  that  the  Cobalt  miners  of  the 
Schneeberg  district  in  the  Saxon  Voigtland  are  very  liable  to  primary 
sarcoma  of  the  lung.  Whether  it  is  due  to  irritation  from  dust  (Adami)  or 
whether  the  endemic  occurrence  points  to  an  infectious  origin  (Strumpell) 
is  uncertain. 

Primary  cancer  of  the  lung  is  generally  looked  upon  as  of  relatively 
rare  occurrence.  According  to  Sailer  and  Torrey2  this  belief  is  not  well 
founded.  By  combining  various  statistics  they  were  able  to  collect 
87,451  autopsies  among  which  130  primary  carcinomas  of  the  lung  were 
found;  that  is,  of  100,000  deaths,  156  are  caused  by  cancer  primary  in 
the  lung. 

Primary  carcinoma  of  the  large  bronchi  is  not  common.  Weller3 
has  collected  90  cases. 

Primary  involvement  of  the  pleura  by  a  carcinoma  is  rare,  there 
being  not  more  than  40  or  50  cases  on  record.  It  is  possible  as  Lord 
suggests,  that  instances  of  the  disease  have  not  infrequently  escaped 
notice  because  of  the  readiness  with  which  it  may  be  confused  with 
thickening  of  the  pleura  due  to  a  chronic  inflammatory  process. 

Primary  sarcoma  of  the  lung  is  much  less  common  than  carcinoma. 
Passler4  found  among  1000  cases  of  malignant  disease  16  cases  of  primary 
carcinoma  of  the  lung  and  4  of  primary  sarcoma;  Seydel5  in  an  analysis 
of  10,829  autopsies  found  20  primary  carcinomas  and  8  sarcomas. 
Rolleston  and  Trevor6  in  3983  autopsies  found  three  primary  sarcomas 

1  Dissert.,  Munch.,  1884. 

2  Penna.  Med.  Jour.,  April,  1913. 

3  Arch.  Int.  Med.,  March,  1913. 

4  Virchow's  Archiv,  Band  cxiv,  S.  191,  1896. 

5  Miinchner  Med.  Woch.,  lvii,  No.  9,  1910. 

6  Brit.  Med.  Jour.,  Feb.  14,  1903. 


DISEASES    OF   THE    LUNGS  499 

and  no  carcinomas  of  the  lung.  Lord1  has  collected  42  cases  in  which 
the  tumor  was  an  undoubted  or  probable  primary  sarcoma. 

Primary  sarcoma  of  the  bronchi  and  pleura  is  even  rarer  than  primary 
carcinoma.  Bernard2  has  collected  24  instances  of  primary  sarcoma  of 
the  pleura. 

The  lungs  may  be  invaded  secondarily  by  a  malignant  growth  by 
direct  extension  from  adjacent  structures  or  by  metastasis  from  some 
distant  organ.  If  the  growth  is  a  carcinoma  the  initial  focus  may  be  one 
of  the  abdominal  viscera  such  as  the  stomach,  liver  or  pancreas,  or  the 
primary  growth  may  be  in  the  prostate.  Metastasis  may  take  place 
by  way  of  the  blood  stream  or  the  lymphatics.  Direct  extension  of  the 
disease  may  occur  when  the  primary  focus  is  in  the  mammary  gland, 
esophagus  or  thyroid  gland.  According  to  Seydel3  metastatic  growths 
in  the  lungs  due  to  cancer  occur  approximately  ten  times  as  frequently 
as  the  primary  growths.  If  the  primary  tumor  is  a  sarcoma,  the  most 
common  origin  of  the  growth  is  the  marrow  of  one  of  the  long  bones.  Two 
tumors  which  histologically  resemble  both  carcinoma  and  sarcoma  are 
the  hypernephromas  and  malignant  deciduomas;  both  the  hyperneph- 
romas and  the  deciduomas  are  especially  apt  to  metastasize  to  the  lungs. 
Of  22  cases  of  hypernephroma  collected  from  the  literature  by  Woolley4 
metastasis  to  the  lungs  occurred  in  13.  Malignant  deciduoma  involves 
the  lungs  secondarily  in  about  50  per  cent,  of  the  cases  and  in  some 
instances  first  manifests  itself  by  coughing,  pleuritic  pain,  hemoptysis, 
and  other  symptoms  referable  to  the  chest.5 

The  Mediastinum. — Owing  to  the  variety  of  the  mediastinal  contents 
and  the  close  relationship  important  structures  bear  to  each  other  in  this 
confined  space  the  occurrence  of  a  tumor  whether  benign  or  malignant 
is  a  serious  matter.  Comparatively  small  benign  tumors  may  produce 
most  serious  symptoms.  Tumors  comprising  the  benign  group  are 
individually  quite  rare  and  the  aggregate  number  of  all  benign  tumors  is 
not  large.  Among  the  benign  tumors  encountered  in  the  mediastinum 
may  be  mentioned  the  following:  fibroma,  lipoma,  chondroma,  myoma, 
simple  cyst  and  dermoid  cyst  and  -teratoma.  Of  the  benign  tumors 
dermoid  cysts  are  by  far  the  most  common.  Hertzle6  has  reported 
6  cases  and  collected  72  cases  from  the  literature. 

By  far  the  commonest  tumors  involving  the  mediastinum  are  those 
comprising  the  malignant  group.  Hare  in  1889  collected  520  instances 
of  mediastinal  affections  and  of  this  number  he  classed  134  as  carcinoma, 
and  98  as  sarcoma.  Many  of  the  cases  included  in  his  analysis  were 
reported  at  a  time  when  the  histological  distinction  between  the  two 
types  of  malignant  tumors  was  not  fully  understood.  Now  that  the 
nature  of  these  tumors  is  better  known  it  is  recognized  that  sarcoma  is 
much  more  common  than  carcinoma.  Endothelioma  rarely  invades  the 
mediastinum  primarily;  it  may  extend  from  a  primary  pleural  growth. 

Morbid  Anatomy. — Benign  tumors  occurring  in  the  lungs  or  bronchi 
are  quite  rare.  They  usually  involve  some  one  of  the  mediastinal  struc- 
tures.    As  has  already  been  stated  a  tumor  involving  either  the  lungs  or 

1  "Diseases  of  the  Bronchi,  Lungs  and  Pleura,"  1915. 

2  Virchow's  Archiv,  cxxi,  156,  1913. 

3  Miinchner  Med.  Woch.,  lvii,  No.  9,  1910. 

4  Amer.  Jour.  Med.  Sc.,  cxxv,  1903. 

5  Stevens,  Am.  Jour.  Med.  Sc.,  cxliv,  1912. 

6  Am.  Jour.  Med.  Sc.,  August,  1916. 


500  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

bronchi  is  usually  malignant.  It  is  frequently  asserted  that  in  primary 
carcinoma  of  the  lungs  and  bronchi  that  the  right  side  is  more  frequently 
involved  than  the  left.  Adler1  states  that  the  difference  in  the  involve- 
ment of  the  two  sides  is  too  small  to  serve  as  a  basis  for  a  theory.  Weller2 
found  that  in  69  cases  the  two  sides  were  involved  with  approximately 
equal  frequency.  Primary  sarcoma  is  also  quite  as  apt  to  occur  on  one 
side  as  the  other. 


Fig.  301. — Colloid  carcinoma. 


Primary  malignant  growths  may  occur  as  a  single  large  tumor  having 
its  origin  in  the  root  of  the  lung  and  extending  into  the  pulmonary  tissue 
or  there  may  be  a  number  of  small  nodules  varying  in  size  from  a  hazel- 
nut to  a  small  orange.  Less  commonly  the  lung  may  be  studded  with 
small  nodules  resembling  miliary  tubercles.  This  widespread  distribu- 
tion, sometimes  referred  to  as  carcinomatosis  or  sarcomatosis,  as  the  case 
may  be,  is  seen  more  frequently  as  a  result  of  metastasis  (Figs.  301  and 
302).     Occasionally  the  growths  are  almost  entirely  subpleural.     Rarely 


1  "Primary  Malignant  Growths  of  the  Lungs  and  Bronchi, 

2  hoc.  cit. 


1911. 


DISEASES    OF    THE    LUNGS 


501 


the  tumor  may  be  single  and  found  projecting  into  the  lumen  of  one  of 
the  larger  bronchi. 

Instead  of  appearing  as  an  isolated  tumor  formation  the  growth  may 
occur  in  an  infiltrating  form.  Wilson  Fox  describes  two  types  of  infiltra- 
tion. First,  it  may  occur  as  a  general  infiltration  in  which  large  areas 
of  the  lung  are  involved.  This  may  be  uniform  or  here  and  there  traces 
of  pulmonary  tissue  may  remain  intact.     The  process  closely  resembles 


Fig.  302. — Sarcomatosis. 


a  dense  tuberculous  infiltration  (see  Fig.  306).  Secondly,  the  infiltra- 
tion may  radiate  from  the  root  of  the  lung  by  way  of  the  lymphatic  chan- 
nels attending  the  bronchi.  Small  or  large  tumor  nodules  or  masses  may 
be  seen  surrounding  the  bronchi.  In  some  instances  the  bronchi  are  but 
little  involved  and  the  lung  tissue  is  chiefly  affected. 

The  carcinomatous  growths  are  of  a  white,  grayish  or  grayish-yellow 
color  and  are  of  firm  consistency.  When  they  occur  in  the  lung  tissue 
they  are  apt  to  be  softer,  and  may  break  down  and  empty  into  a  bronchus 
thus  forming  a  cavity.  The  most  common  form  of  cancer  is  that  com- 
posed of  cylindrical  cells.     Metastases  to  other  organs  in  the  body  are 


502         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

quite  common.     Bronchial  carcinoma  is  especially  prone  to  give  rise  to 
metastasis  to  the  brain  (Weller). 

Sarcomatous  growths  usually  occur  in  the  form  of  isolated  tumors 
which  may  be  single  or  multiple.  Large  single  growths  sometimes  attain 
the  size  of  an  infant's  head  (Fig.  303).  Infiltrating  growths  are  less 
common  than  with  carcinoma.  The  tumors  are  usually  somewhat  soft 
and  of  a  grayish,  whitish  or  reddish  color.  Any  type  of  sarcoma  may 
be  found  but  the  small  round-celled  variety  is  the  most  common.     Meta- 


Fig.   303. — Large  metastatic  growth  in  right  lung.     Primary  growth  a  hypernephroma  of 

left  kidney. 

stasis  occurs  but  is  less  common  than  in  the  case  of  carcinoma.  Other 
changes  in  the  lungs  may  consist  of  congestion  or  aletectasis  in  the  tissue 
immediately  around  the  tumor  masses.  Less  frequently  broncho- 
pneumonia, abscess  or  gangrene  of  the  lung  may  arise.  A  pleural  effu- 
sion is  not  uncommon  especially  when  the  pleura  is  involved.  Effusions 
which  arise  as  the  result  of  malignant  disease  not  only  have  a  marked 
tendency  to  reaccumulate  after  removal  but  are  also  often  hemorrhagic 
in  character.     The  last  feature  is  always  suggestive  of  malignancy. 


DISEASES    OF    THE    LUNGS  503 

While  there  are  some  who  believe  the  association  of  tuberculosis  and 
malignant  disease  of  the  lungs  is  not  infrequent  the  majority  of  observers 
hold  the  view  that  the  two  diseases  rarely  coexist.  Among  the  662 
autopsies  at  the  Phipps  Institute  there  has  been  no  instance  in  which 
the  two  diseases  occurred  together.  K.  Wolf1  has  reported  31  cases  of 
malignant  disease  of  the  lungs  in  13  of  which  tuberculosis  also  existed. 
Shaw2  however,  accepts  but  8  of  these  as  being  even  possible  and  regards 
most  of  them  as  doubtful.  He  furthermore  holds  that  the  only  true  test 
is  the  demonstration  of  tubercle  bacilli.  Among  60  cases  of  malignant 
disease  studied  by  Ross3  there  were  2  cases  in  which  tubercle  bacilli 
were  found  in  the  sputum.  He  states  that  the  frequency  of  healed 
tuberculous  lesions  found  at  the  autopsy  is  of  no  significance  as 
they  are  found  with  equal  frequency  in  individuals  dying  of  other 
diseases. 

Secondary  involvement  of  the  lungs  may  occur  as  the  result  of  exten- 
sion from  a  nearby  source  or  as  the  result  of  metastasis  from  a  distant- 
focus  and  while  the  lungs  may  escape  it  is  rare  for  the  metastatic  growths 
to  occur  in  the  lungs  alone.  In  the  majority  of  cases  the  primary  tumor 
is  located  in  the  breast,  esophagus,  stomach,  liver,  peritoneum,  testes 
and  bones.  The  secondary  growths  usually  occur  in  the  form  of  large 
or  small  isolated  nodules.  There  may  be  only  one  or  they  may  be  mul- 
tiple. Rarely  the  secondary  invasion  takes  the  form  of  a  diffuse  infiltra- 
tion and  still  more  rarely  carcinoma  may  occur  in  a  miliary  form  (car- 
cinomatosis). As  a  rule,  the  histology  of  the  secondary  tumors  is  that 
of  the  parent  growth. 

Malignant  disease  involving  the  pleura  may  be  primary  or  secondary 
as  the  result  of  direct  extension  from  the  lung  or  as  part  of  a  general 
metastasis.  When  primary  the  most  common  form  is  an  endothelioma. 
When  malignant  disease  affects  the  pleura  primarily  it  manifests  itself 
in  two  forms.  First,  it  may  consist  of  an  infiltrating  process  which  greatly 
increases  the  thickness  of  the  pleura.  Not  uncommonly  the  parietal 
layer  is  involved  exclusively  without  implication  of  the  chest  structures 
but  extending  into  the  mediastinal -tissues  (Wilson  Fox).  If  limited  to 
the  pleura  the  change  may  be  attributed  to  simple  inflammatory  thick- 
ening. Secondly,  the  growth  may  consist  of  large  or  small  nodules 
in  both  layers  of  the  pleura  (Fig.  304).  The  infiltrating  and  nodular 
forms  may  occur  together.  Direct  extension  of  the  disease  from  the 
lungs  or  mediastinum  may  cause  the  same  changes. 

Mediastinal  tumors  of  the  benign  types  are  of  pathological  interest 
only  and  during  life  are  not  to  be  distinguished  one  from  the  other  with 
the  exception  of  dermoid  cysts. 

The  sarcomatous  and  carcinomatous  growths,  on  the  other  hand, 
present  characteristics  which  render  it  possible  to  make  a  correct  diag- 
nosis of  the  malignant  nature  of  the  tumor  in  many  instances.  A  sarcoma 
may  spring  from  the  connective  tissue  in  the  mediastinum,  the  peribron- 
chial or  the  mediastinal  lymph  nodes.  Tumors  in  this  situation  are 
usually  of  the  spindle-celled  type  or  lympho-sarcoma,  the  latter  being 
the  more  common.  The  tumor  usually  consists  of  a  solid  mass  which  by 
its  extension  exerts  more  and  more  pressure  on  the  mediastinal  contents. 

1  Fortschritte  der  Medicin,  1895,  xiii. 

2  Brit.  Med.  Jour.,  1901,  i,  1831. 

3  Edinburgh  Med.  Jour.,  December,  1914. 


504         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

It  may  extend  beyond  the  limits  of  the  mediastinum  and  invade  the  lungs 
secondarily.  Tumors  situated  in  the  anterior  mediastinum  very  often 
cause  a  bulging  of  the  chest  wall  in  the  median  line  or  to  one  side  or  the 
other  of  the  sternum. 

The  consistency  of  these  tumors  is  moderately  firm  and  they  are  of  a 
gray,  yellowish-gray  or  reddish  color.  Rapidly  growing  tumors  are  apt 
to  be  quite  soft  and  friable. 

A  primary  carcinoma  is  not  common  in  the  mediastinum.  If  we 
eliminate  cases  which  should  be  classed  as  sarcomas,  lympho-sarcomas, 
secondary  carcinomas,  pleural  endotheliomas,  and  bronchial  carcinomas, 


Fig.  304. — Sarcomatosis  of  pleura 


few  cases  remain  (Christian).  A  mediastinal  growth  occurring  in  middle 
aged  people  and  which  tends  to  spread  to  surrounding  structures  as  indi- 
cated by  the  symptoms,  physical  signs  and  roentgenograms,  is  probably  a 
carcinoma.  The  final  proof,  however,  must  rest  on  the  histological 
examination. 

Symptoms. — From  the  clinical  standpoint  the  benign  tumors  can  be 
dismissed  from  consideration.  With  one  exception  they  are  of  patho- 
logical interest  only.  Dermoid  cysts  will  be  considered  separately. 
The  symptoms  of  malignant  growths  may  be  divided  into  three  classes: 
(1)  Those  which  occur  in  all  forms;  (2)  constitutional  symptoms;  and 
(3)  special  symptoms  which  indicate  either  the  nature  or  the  location  of 
the  growth. 


DISEASES    OF    THE    LUNGS  505 

1.  Onset. — The  onset  majT  be  insidious  with  a  gradual  failure  of 
health  or  it  may  be  more  or  less  acute  with  severe  symptoms  and  all 
the  evidences  of  a  rapid  decline. 

Dyspnea,  cough,  expectoration  and  pain  are  the  most  common 
symptoms. 

Dyspnea  is  one  of  the  earliest  and  one  of  the  most  common  symptoms 
encountered  in  intrathoracic  growths.  It  may  be  due  to  destruction  of 
the  pulmonary  tissue  by  the  tumor.  On  the  other  hand,  it  is  to  be  borne 
in  mind  that  intense  dyspnea  may  occur  out  of  all  proportion  to  the 
amount  of  damage  demonstrable  in  the  lungs.  Cyanosis  is  commonly 
present  under  these  circumstances.  In  a  case  seen  in  the  Phipps  Insti- 
tute the  patient's  only  symptoms  were  intense  dyspnea,  cyanosis  and  a 
slight  cough.  Examination  of  the  lungs  revealed  a  few  scattered  rales 
on  both  sides,  but  no  localizing  signs.  The  heart  showed  nothing  ab- 
normal and  the  pulse  rate  was  under  90.  At  the  autopsy  not  more  than 
a  half  dozen  nodules,  the  size  of  an  English  walnut,  were  found  in  each 
lung.  The  primary  disease  consisted  of  a  small  scirrhous  carcinoma  in 
the  left  breast.  The  cause  of  the  dyspnea  and  cyanosis  in  such  cases  is 
not  understood.  Dyspnea  may  occur  as  the  result  of  pressure  on  the 
larger  bronchi  or  trachea  in  the  case  of  mediastinal  tumors.  In  some 
instances  it  is  believed  to  be  due  to  pressure  on  nerve  trunks.  It  may  be 
caused  also  as  the  result  of  a  large  complicating  pleural  effusion. 

The  difficulty  in  breathing  is  usually  constant  but  it  may  be  par- 
oxysmal in  character.  Occasionally  it  is  severe  enough  to  be  termed 
orthopnea. 

In  addition  to  the  dyspnea  the  breath  sounds  may  have  a  stridulous 
sound  as  the  result  of  pressure  on  the  main  bronchi  or  trachea.  Hoarse- 
ness may  occur  also  if  the  left  recurrent  laryngeal  nerve  is  involved. 

Cough. — This  is  an  almost  constant  symptom;  in  Walshe's  experience 
it  is  invariably  present  when  the  lungs  are  involved.  .  It  may  be  due 
to  an  associated  bronchitis  or  as  the  result  of  pressure.  It  varies  greatly 
in  severity. 

Expectoration. — The  sputum  may.be  mucoid,  mucopurulent,  blood- 
streaked  or  hemorrhagic.  The  presence  of  blood  in  the  sputum  or  the 
occurrence  of  small  hemoptyses  are  extremely  common  when  the  lungs 
are  involved.  Occasionally  the  expectorated  blood  is  thick,  dark  in 
color  and  closely  resembles  currant  jelly.  When  present  it  is  highly 
suggestive  of  malignant  disease. 

In  cases  of  suspected  malignant  disease  of  the  lungs  and  bronchi  the 
sputum,  especially  when  hemorrhagic  in  character,  should  be  examined 
both  macroscopically  and  microscopically.  As  the  result  of  necrosis  and 
ulceration  bits  of  the  tumor  mass  may  be  discharged  in  the  sputum  and 
are  seen  as  whitish,  grayish  or  pinkish-colored  particles  or  shreds.  These 
shreds  may  resemble  small  pieces  of  washed-out  meat  (Salter).  In  the 
stained  specimen  there  may  be  present  a  large  number  of  cells,  either 
isolated  or  in  clusters,  which  are  very  suggestive  of  malignant  disease. 
So  too  is  the  presence  of  refractive  spherical  bodies  containing  fatty 
granules  (Lenhartz).  In  a  case  seen  several  years  ago  the  presence  of 
numerous  clusters  of  large  cells  in  the  sputum  gave  the  first  clue  as  to 
the  nature  of  the  trouble. 

Pain  may  be  the  first  symptom.  It  is  usually  an  indication  that  the 
pleura  is  involved  either  primarily  or  secondarily.     It  may  arise,  how- 


506  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

ever,  as  the  result  of  pressure.  Tumors  in  the  mediastinum  may,  by 
extending  forward,  give  rise  to  pain  similar  to  that  occurring  in  thoracic 
aneurism.  The  pain  may  be  constant  or  paroxysmal.  In  the  pleural 
cases  it  may  have  all  the  features  of  an  acute  pleurisy  while  in  the 
mediastinal  cases  it  may  produce  a  dull  boring  pain  due  to  pressure  and 
erosion.  Neuralgic  pain  may  also  occur  if  the  intercostal  nerves  are 
involved  and  associated  with  this  there  may  be  herpes  zoster.  In  some 
instances  the  pain  is  objective  entirely  and  can  be  elicited  only  by  pressure 
with  the  palpating  finger. 

2.  Constitutional  Symptoms. — Malignant  disease  of  the  thoracic 
organs  give  rise  to  the  same  constitutional  symptoms  as  do  malignant 
growths  in  any  portion  of  the  body.  The  progress  of  the  disease  may  be 
exceedingly  rapid  or  it  may  be  relatively  slow.  Wilson  Fox  states  that 
the  duration  of  the  disease  ranges  from  four  years  to  three  weeks  while 
Walsh  found  the  maximum  length  of  time  to  be  twenty-seven  months  and 
the  minimum  three  and  a  half  months.  The  acuteness  of  the  disease 
depends  to  a  large  extent  on  the  rate  of  the  growth  and  the  amount  of 
pressure  it  exerts.  In  the  case  of  mediastinal  growths  the  disease  may 
have  been  present  for  some  time  before  pressure  symptoms  finally  direct 
attention  to  its  presence.  In  practically  all  cases  there  is  a  more  or  less 
rapid  loss  in  weight  and  strength  and  the  patient  becomes  cachectic. 
Night  sweats  are  common  and  an  irregular  type  of  fever  is  frequently 
present  (Fig.  305).  In  common  with  other  chronic  wasting  diseases, 
anemia,  malaise,  a  capricious  appetite  and  digestive  disturbances  are 
common. 

Metastases  to  other  portions  of  the  body  may  take  place  and  entirely 
mask  the  pulmonary  lesion.  Metastasis  to  the  brain  is  not  an  uncommon 
occurrence  in  tumors  originating  in  the  bronchi.  Death  finally  takes 
place  as  the  result  of  asthenia,  hemorrhage  or  an  acute  infection. 

3.  Pressure  Symptoms. — For  the  most  part  the  special  or  localizing 
symptoms  result  from  the  pressure  exerted  by  mediastinal  growths. 
Pressure  on  one  of  the  pneumogastric  nerves  may  give  rise  to  paroxysmal 
dyspnea  or  cough  and  occasionally  to  attacks  of  vomiting.  The  pulse 
may  be  increased  in  frequency  or  occasionally  it  may  be  greatly  retarded. 
If  the  recurrent  laryngeal  nerves,  especially  the  left,  are  involved  by  the 
growth  there  may  be  hoarseness  or  aphonia.  Pressure  on  the  sympathetic 
may  lead  to  inequalities  of  the  pupils,  that  on  the  affected  side  being 
contracted  or  dilated. 

Symptoms  referable  to  the  blood-vessels  are  not  unusual  and,  as  a 
rule,  the  veins  are  more  frequently  affected  than  the  arteries.  In  not  a 
few  cases  inequality  of  the  radial  arteries  has  been  noted.  As  the  result 
of  pressure  on  the  superior  vena  cava  or  one  of  its  main  tributaries,  the 
veins  over  the  upper  part  of  the  chest  may  become  greatly  dilated,  vari- 
cose and  tortuous.  In  addition  the  face,  upper  part  of  the  thorax  and 
the  arms  may  become  cyanosed,  swollen,  and  edematous.  At  times  the 
tissues  of  the  neck  and  chest  wall  become  brawny  and  very  tense.  The 
evidences  of  venous  stasis  may  be  limited  to  one  side  or  may  involve 
both  sides.  As  the  result  of  the  interference  with  the  returning  blood 
cerebral  symptoms  may  occur,  such  as  headache,  vertigo  and  som- 
nolence. These  symptoms  are  apt  to  be  increased  by  exertion  and,  in 
some  instances,  are  among  the  first  manifestations  of  an  intrathoracic 
growth. 


DISEASES    OF    THE    LUNGS 


507 


Pressure  on  the  esophagus  may  give  rise  to  difficulty  in  swallowing. 

Dermoid  Cyst. — As  previously  stated  this  growth  is  the  only  one  of 

the  benign  tumors  which  is  of  clinical  interest.     The  most  common  situa- 


o 


tion  of  tumors  of  this  type  is  in  the  upper  part  of  the  chest  behind'the 
sternum.  The  cyst  or  tumor,  as  the  case  may  be,  may  exist  without 
giving  rise  to  any  manifestations  whatever.  When  symptoms  are  present 
they    are  the  same  as  those  arising  from  any  form  of  tumor,  namely, 


508  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

cough,  expectoration,  pain  and  pressure  symptoms.  When  it  can  be 
demonstrated  that  a  tumor  is  the  cause  of  the  above  symptoms  a  dermoid 
cyst  or  tumor  is  to  be  suspected  if  the  progress  of  the  disease  is  slow  and 
long  drawn  out.  This  is  in  contrast  to  malignant  tumors  which  are 
characterized,  as  a  rule,  by  a  rapid  rate  of  growth.  The  most  distinc- 
tive feature  of  dermoid  cyst  is  the  presence  of  hair  in  the  sputum.  In 
some  instances  the  cyst  ruptures  through  the  chest  wall  in  which  case 
particles  of  hair  may  be  detected  in  the  discharge  from  the  fistulous 
opening. 

Secondary  Growths.- — The  symptoms  of  secondary  malignant  growths 
are  essentially  the  same  as  in  the  case  of  the  primary  growths.  The 
diagnosis  is  oftener  easier,  however,  because  of  the  existence  of  a  primary 
growth  or  the  knowledge  that  a  malignant  tumor  has  been  removed. 
Under  these  circumstances  respiratory  symptoms  which  might  otherwise 
be  misinterpreted  are  recognized  as  being  due,  in  all  probability,  to 
secondary  malignant  growths. 

Physical  Signs. — Generally  speaking  the  abnormal  physical  signs 
produced  by  intrathoracic  tumors  are  elicited  over  the  lower  half  of  the 
chest  except  in  the  case  of  mediastinal  growths  which,  although  occurring 
most  frequently  in  the  upper  half  of  the  thorax,  are  situated  behind  or 
just  to  one  side  of  the  sternum.  The  apices  are  rarely  involved  except 
as  part  of  a  general  invasion  of  the  entire  lung. 

Inspection. — This  may  be  entirely  negative.  In  the  case  of  medias- 
tinal involvement  pressure  signs  may  be  detected.  The  pupils  may  be 
unequal  as  the  result  of  pressure  on  the  sympathetic.  Dilatation  of  the 
veins  in  the  chest  is  common.  Usually  the  veins  over  the  upper  part  of 
the  thorax  are  the  ones  involved  but  the  veins  of  the  arms,  lower  thorax 
and  upper  abdomen  may  be  involved  also.  Venous  stasis  may  also 
manifest  itself  by  cyanosis  of  the  lips  and  ears.  Edema  of  the  chest 
wall  also  occurs.  If  the  growth  is  in  the  anterior  mediastinum  the  upper 
part  of  the  sternum  may  present  a  bulging  point  and  this  external  tumor 
may  pulsate.  The  pulsation  is  due  to  transmission  of  the  aortic  impulse. 
Localized  bulging  may  be  noted  also  in  other  portions  of  the  chest, 
especially  in  rapidly  growing  tumors. 

If  the  growth  is  unilateral  the  affected  side  will  be  seen  to  expand 
poorly.  The  apex  beat  of  the  heart  may  be  displaced.  In  some  in- 
stances extreme  clubbing  of  the  fingers  with  or  without  enlargement  of 
the  long  bones  (hypertrophic  pulmonary  osteo-arthopathy)  may  develop 
very  rapidly  (see  Fig.  3).  If  the  tumor  originates  in  one  of  the  large 
bronchi  direct  inspection  of  the  growth  is  possible  through  the  broncho- 
scope. 

Palpation.- — Over  the  involved  area  of  the  lungs  the  tactile  fremitus 
is  usually  absent  or  greatly  diminished.  Palpation  also  serves  to  em- 
phasize differences  in  the  expansion  of  the  two  sides.  Firm  pressure 
with  the  finger  tips  will  often  elicit  tender  spots,  especially  if  the  pleura 
is  involved.  Pressure  with  the  finger  tips  also  may  reveal  the  presence 
of  edema  of  the  chest  wall.  In  some  instances  the  superficially  placed 
lymph  nodes  may  show  enlargement  as  the  result  of  metastasis. 

Percussion. — Areas  of  absolute  dulness  may  occur  at  any  point  and 
are  dependent  on  the  nature  and  extent  of  the  growth.  Dulness  is  most 
commonly  encountered  directly  over  or  to  one  side  of  the  sternum,  in  the 
interscapular  region  and  over  the  base  of  the  lungs. 


DISEASES    OF   THE    LUNGS  509 

Auscultation.- — If  the  growth  is  limited  to  the  mediastinum  there  may 
be  no  noticeable  auscultatory  change.  If  pressure  is  exerted  on  the 
trachea  or  large  bronchi  the  breath  sounds  may  have  a  harsh  and  stridu- 
lous  character.  Involvement  of  the  pulmonary  tissue  either  primarily 
or  secondarily  may  give  rise  to  broncho-vesicular,  bronchial  or  suppressed 
breath  sounds.  In  the  pulmonary  cases  rales  are  nearly  always  heard 
as  the  result  of  an  associated  bronchitis.  With  involvement  of  the 
pleura  the  breath  and  voice  sounds  are  usually  distant  and  suppressed. 

Diagnosis. — The  recognition  of  primary  malignant  growths  is  not 
easy.  This  is  due  in  part  to  their  rarity  and  in  part  to  the  fact  that  the 
symptoms  to  which  they  give  rise  are  encountered  in  the  more  common 
thoracic  affections.  Secondary  malignant  disease  of  the  lungs  on  the 
other  hand,  is,  in  the  majority  of  instances,  easily  recognized  providing 
there  is  present  a  primary  growth  or  the  knowledge  that  such  a  growth 
has  been  removed.  If,  however,  the  primary  growth  escapes  detection 
and  gives  rise  to  no  symptoms  metastasis  to  the  lungs  may  occur  without 
the  true  nature  of  the  trouble  being  suspected.  Pressure  symptoms 
should  always  suggest  an  intrathoracic  growth  especially  when  aneurism 
can  be  excluded.  The  only  distinctive  feature  of  these  growths  is  the 
presence  of  numerous  large  cells,  singly  or  in  clusters,  in  the  sputum  and 
this  is  available  in  the  lung  cases  only. 

Tuberculosis. — Instances  of  malignant  disease  are  not  infrequently 
seen  in  institutions  for  the  care  of  tuberculous  patients.  Washburn1 
reports  the  finding  of  5  cases  of  malignant  disease  of  the  lungs  out  of 
198  autopsies  at  the  Boston  Consumptives  Hospital.  The  fact  that 
intrathoracic  growths  almost  invariably  give  rise  to  symptoms  which 
are  associated  constantly  with  tuberculosis  is  responsible  for  this.  The 
persistent  absence  of  tubercle  bacilli  in  the  sputum,  the  marked  dyspnea 
and  the  localization  of  the  physical  signs  in  the  anterior  mediastinum,  about 
the  roots  or  at  the  bases  of  the  lungs  should  serve  as  warnings.  Tubercu- 
losis is  either  localized  at  the  summit  of  the  lung  or  if  the  whole  lung  is 
diseased,  the  most  destructive  lesions  are  found  where  the  process  first 
started,  namely,  at  the  apex.  Occasionally  the  malignant  growth  is 
confined  to  the  upper  lobe  of  the  lung  (Fig.  306).  In  such  cases  a  diag- 
nosis of  tuberculosis  can  be  avoided  only  by  giving  heed  to  the  negative 
sputum  examinations. 

Bronchitis. — Occasionally  cases  of  malignant  disease  are  encountered 
in  which  there  are  no  localizing  signs  in  the  lungs  and  all  that  can  be 
detected  is  the  presence  of  scattered  rales.  If  the  sputum  is  blood- 
streaked  and  does  not  contain  tubercle  bacilli  and  in  addition,  the  heart 
shows  no  evidence  of  failing  compensation,  malignant  disease  should 
be  thought  of.  Extreme  dyspnea  and  cyanosis  occurring  in  a  case  pre- 
senting the  physical  signs  of  a  simple  bronchitis  are  very  suggestive  of 
malignant  disease. 

Chronic  inflammatory  conditions  of  the  lung  are  to  be  distinguished 
from  malignant  disease  by  their  long  duration  and  the  absence  of  severe 
constitutional  symptoms. 

Pleural  Effusion. — The  frequency  with  which  malignant  disease  is 

mistaken  for  a  pleural  effusion  has  long  been  recognized.     The  causes  of 

error  lie  in  the  bulging  of  the  affected  side,  the  flat  percussion  note  and 

the  absence  of  the  voice  and  breath  sounds.     Pleural  effusion  rarely 

1  Boston  Med.  and  Surg.  Jour.,  October  28,  1915. 


510  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

gives  rise  to  pressure  symptoms  although  the  displacement  of  the  thoracic 
viscera,  especially  the  heart,  is  usually  more  marked  than  in  cases  of 
malignant  disease.  The  presence  or  absence  of  Grocco's  triangle  is 
sometimes  of  service  in  distinguishing  the  two  conditions.  The  most 
certain  method  is  the  use  of  an  exploring  needle.  In  addition  the  X-rays 
should  be  utilized  in  all  doubtful  cases. 

If  malignant  disease  and  pleural  effusion  coexist  the  exciting  cause  of 
the  fluid  may  be  overlooked.     A  hemorrhagic  effusion  while  not  pathog- 


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Fig.  306. — Malignant  disease  of  upper  lobe.     Patient  from  whom  this  specimen  came  had 
been  treated  in  several  sanatoria  for  tuberculosis.      (Jefferson  Medical  College  Museum.) 


nomonic  of  malignant  disease,  is  suggestive.  Ross1  in  a  study  of  60 
cases  of  malignant  disease  involving  the  mediastinum  stated  that  there 
was  an  effusion  in  29  and  of  this  number  15  were  hemorrhagic. 

Encysted  effusions  may  be  mistaken  for  malignant  disease  and  vice 
versa.  The  differentiation  rests  for  the  most  part,  on  the  use  of  the  explor- 
ing needle,  the  X-ray  examination  and  the  course  of  the  disease. 

Pericardial  Effusion. — A  tumor  involving  the  anterior  mediastinum 
at  times  assumes  the  pyramidal  shape  of  a  pericardial  effusion  (Fig.  307). 

1  Edinburgh  Med.  Jour.,  December,  1914. 


DISEASES    OF    THE    LUNGS 


511 


In  case  of  an  effusion  the  cardiac  symptoms  are  usually  marked  while 
pressure  symptoms  are  absent;  the  reverse  is  true  in  cases  of  tumor.  As 
in  all  mediastinal  affections  the  X-rays  are  invaluable. 

Aneurism  of  the  Arch  of  the  Aorta. — Many  of  the  symptoms  and  signs 
of  aneurism  also  occur  in  tumors  involving  the  anterior  mediastinum. 
Thus  the  tumor  may  cause  a  bulging  of  the  chest  wall  over  the  site  in 
which  aneurisms  commonly  occur  and  this  bulging  tumor  may  be  seen 


Fig.  307. 


-Tumor  in  anterior  mediastinum.     Area  of  percussion  dulriess  resembled  that  in 
pericardial  effusion. 


to  pulsate  as  the  result  of  transmission  of  the  normal  aortic  impulse 
through  the  tumor.  Furthermore,  the  tumor  may  cause,  by  pressure 
on  the  main  arterial  branches,  an  inequality  of  the  pulses.  In  the  case 
of  a  tumor  the  pulsation  is  not  expansile  in  character,  a  thrill  is  rarely 
present  and  a  diastolic  murmur  is  also  very  rare.  In  young  individuals 
aneurism  is  much  less  common  than  tumor.  An  X-ray  examination 
should  always  be  made  in  doubtful  cases. 


512  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Leukemia  and  Hodgkin's  Disease. — Involvement  of  the  mediastinal 
lymph  nodes  often  masks  the  picture  of  these  conditions.  The 
physical  signs  are  those  of  a  mediastinal  tumor.  The  presence  of  en- 
larged lymph  nodes  elsewhere  and  the  blood  picture  serve  to  differentiate 
them.     The  X-rays  will  also  show  the  enlarged  lymph  nodes  (Fig.  308) . 


Fig.   308. — Mediastinal  adenitis  (in  myelogenous  leucemia).      {Dr.  D.  R.  Bowen.) 

Enlargement  of  the  Thymus 

A  number  of  terms  have  been  employed  to  indicate  an  increase  in 
the  size  of  the  thymus:  Persistence  of  the  thymus,  hyperplasia,  hyper- 
trophy, status  lymphaticus,  status  thymico-lymphaticus,  lymphaiism, 
thymic  tracheostenosis. 

General  Considerations.- — Little  is  known  concerning  the  thymus  and 
there  is  considerable  difference  of  opinion  as  to  its  histological  status. 
By  some  it  is  classed  among  the  ductless  glands,  although  structurally  it 
has  little  resemblance  to  these  organs;  others  look  upon  it  as»an  epithelial 
structure;  the  majority  of  observers,  however,  consider  the  thymus  as 
belonging  to  the  lymphoid  organs.  At  birth  the  thymus  is  seen  to  con- 
sist of  a  pinkish  mass  lying  in  the  upper  part  of  the  anterior  mediastinum 
and  extending  from  just  below  the  thyroid  to  the  pericardium.  It  is 
composed  of  two  long,  flat  lobes  more  or  less  fused  together,  although 
often  separated  by  a  fissure.  It  is  enclosed  in  a  connective  tissue  capsule 
that  sends  in  trabecular  dividing  it  into  lobes  and  lobules.  The  sac  is 
loosely  attached   to   the  sternum  in  front,  laterally  to  the  pleurae,  and 


DISEASES    OF    THE    LUNGS  513 

posteriorly  is  firmly  united  to  the  pericardium.  Prolongations  also 
connect  it  with  the  trachea,  bronchi  and  pulmonary  veins.  At  birth 
the  thymus  weighs  from  7  to  10  grams.  According  to  Warthin  glands 
weighing  20  or  30  grams  are  to  be  looked  upon  as  being  abnormally 
enlarged.  The  thymus  gradually  increases  in  size  up  to  the  second  year. 
It  may  then  remain  stationary  or  gradually  undergo  atrophy.  With 
the  advent  of  puberty  it  undergoes  rapid  involution  and  by  the  twentieth 
vear  is  represented  by  a  mass  of  fibrous  and  fatty  tissue  (see  Figs.  65, 
111,  113,  114). 

The  function  of  the  organ  is  equally  obscure.  Krehl  is  of  the  opinion 
that  its  entire  anatomical  development,  its  persistence  through  adoles- 
cence, its  regression  as  growth  nears  completion — all  speak  for  its  role 
in  the  building  of  the  body.  But  although  there  has  been  considerable 
experimental  work  done  in  the  endeavor  to  throw  light  upon  the  subject, 
nothing  definite  is  known.  It  has  been  shown  experimentally  that  there 
is,  apparently,  some  relationship  between  the  thymus  and  the  testes, 
castration  delaying  the  involution  of  the  thymus  while  removal  of  the 
latter  causes  a  more  rapid  development  of  the  testes.  It  is  also  believed 
that  the  organ  is  concerned  in  the  development  of  the  osseous  and  central 
nervous  systems  and  is  in  some  way  related  to  the  blood-making  organs. 

Although  the  thymus  may  be  the  seat  of  disease  such  an  occurrence 
is  extremely  rare.  Clinically  the  thymus  is  of  interest  chiefly  because 
of  enlargement  of  the  organ. 

Etiology. — The  condition  is  encountered  for  the  most  part  in  infants 
and  young  children  but  it  may  occur  in  adults.  In  some  cases  there  is 
apparently  a  relationship  between  the  hypertrophy  of  the  gland  and 
other  disease  processes,  indicating  possibly  a  compensator}'  action.  In  a 
few  instances  the  enlargement  may  be  associated  with  an  acute  infection. 
In  many  cases  there  is  no  adequate  explanation.  Infants  who  die  sud- 
denly after  an  attack  of  cl^yspnea  or  who  are  found  dead  in  bed  are  often 
the  subjects  of  enlarged  thymus.  Clinically  it  is  important  to  bear  in 
mind  that  adenoids  and  thymus  hyperplasia  are  sometimes  associated. 
It  has  long  been  known  that  enlargement  of  the  thymus  often  compli- 
cates any  kind  of  goitre.  Crotti1  has  reported  6  cases  (5  adults,  1  infant) 
in  which  this  combination  occurred.  He  urges  that  all  goitre  cases  and 
especially  those  suffering  from  hyperthyroidism,  should  be  examined 
for  the  presence  of  an  enlarged  thymus,  as  the  sudden  death  which  occa- 
sionally takes  place  in  Graves'  disease  may  be  due  to  this  cause.  Matti2 
collected  from  the  literature  133  cases  of  hyperthyroidism  in  which  an 
autopsy  had  been  held,  and  in  98  cases  (74  per  cent.)  a  hyperplastic 
thymus  was  found.  Hector  MacKenzie  is  of  the  opinion  that  the  associ- 
ation of  Graves'  disease  and  enlargement  of  the  thymus  is  too  frequent 
to  be  accidental.  Occasionally  enlargement  of  the  thymus  occurs  in 
leukemia. 

Morbid  Anatomy. — In  addition  to  enlargement  of  the  thymus  there 
may  be  alterations  in  adjacent  structures  due  to  pressure  and  develop- 
mental changes.  In  the  majority  of  cases  of  enlargement  of  the  thymus 
the  pathological  picture  is  that  of  ''status  lymphaticus."  The  children 
are  large  for  their  age  and  often  have  large  heads.  The  body  t';M  is 
usually  increased.     Anemia  is  more  or  less  well  marked  and  the  facies 

1  Jour.  Am.  Med.  Assoc,  Jan.  11,  L913;  Ibid,  Feb.  22,  L913. 

2  Deal.  Zeit.f.  Chir.,  1912,  cxii. 


514         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

present  a  pasty  appearance.  The  lymphoid  structures  throughout  the 
body  are  usually  increased.  The  external  and  internal  lymph  nodes, 
tonsils  and  solitary  follicles  in  the  intestines  are  hyperplastic  and  ade- 
noids are  commonly  present. 

The  pressure  of  an  enlarged  thymus  is  exerted,  for  the  most  part,  on 
the  trachea  which  in  extreme  cases  may  be  almost  completely  stenosed. 
Pressure  may  also  be  exerted  on  the  heart  and  to  this  may  be  ascribed 
some  of  the  cases  of  sudden  death.  When  respiratory  symptoms  are 
present  they  are  always  due  to  pressure  on  the  trachea  which  is  often 
severe  enough  to  cause  death  by  suffocation.  In  those  cases  in  which 
there  is  no  pressure  on  the  trachea  death  probably  is  due  to  toxemia 
resulting  from  an  overproduction  of  the  internal  secretion  of  the  thymus 
and  lymph  glands  (Osier). 

Symptoms. — In  not  a  few  cases  there  are  no  premonitory  symptoms, 
or  if  they  have  been  present  they  have  been  overlooked.  Sudden  death 
from  enlargement  of  the  thymus  is  not  an  uncommon  event  in  young 
children  who  have  given  no  previous  evidence  of  ill  health.  In  children 
who  are  believed  to  have  been  "overlaid"  by  the  mother  the  true  cause 
of  death  is  to  be  found,  in  some  instances,  in  enlargement  of  the  thymus. 

Occasionally  a  new-born  child  is  extremely  cyanotic  and  the  respira- 
tions labored  and  noisy.  It  may  be  revived  but  dies  in  a  few  hours.  In 
such  cases  a  greatly  enlarged  thymus  is  found  to  be  present. 

Sudden  death,  the  underlying  cause  of  which  is  an  enlarged  thjmius, 
may  also  follow  a  severe  fright,  great  emotion,  a  surgical  operation  or 
anesthesia.  Warthin  believes  that  a  large  proportion  of  deaths  occur- 
ring in  surgical  anesthesia  are  due  to  enlargement  of  the  thymus.  Sus- 
pected cases  should  be  carefully  examined  before  submitting  them  to  an 
operation. 

The  most  striking  and  important  symptom  of  hyperplasia  of  the 
thymus  is  dyspnea  due,  in  part,  to  diminution  of  space  in  the  upper 
thorax  and,  in  part,  to  varying  degrees  of  stenosis  of  the  trachea.  The 
severity  of  the  dyspnea  varies  tremendously.  It  may  be  nothing  more 
than  a  mild  form  of  stridor  or  it  may  be  fulminating  in  character  and  cause 
death  in  a  few  minutes.  Between  these  extremes  all  possible  grades  may 
occur.  The  difficulty  in  breathing  often  manifests  itself  in  the  first  weeks 
or  months  of  life  and  diminishes  after  the  second  year  at  which  time  the 
gland  begins  to  undergo  involution. 

The  dyspnea  may  consist  of  a  stridorous  type  of  breathing  which 
may  be  audible  at  a  distance.  It  is  most  marked  during  inspiration  but 
may  occur  during  expiration  also.  This  type  of  breathing  may  remain 
stationary  or  it  may  become  progressively  worse  as  the  pressure  on  the 
trachea  becomes  greater. 

In  more  severe  cases  the  disturbance  in  breathing  is  often  paroxysmal 
or  asthmatic  in  character.  The  pseudoasthmatic  attacks  may  occur  in 
cases  with  persistent  stridor  or  they  may  develop  when  there  have  been 
no  previous  symptoms.  This  type  of  breathing  was  first  described  by 
Kopp  and  is  often  referred  to  as  Kopp's  asthma.  A  fatal  issue  may 
follow  the  first  of  these  attacks  but  as  manj^  as  twenty  or  thirty  may 
occur.  "In  paroxysmal  dyspnea,  the  child  suddenly  suffocates  and 
becomes  cyanotic.  The  stridor  is  extremely  marked,  respiration  becomes 
accelerated  and  there  is  a  sucking  in  of  the  suprasternal  and  infrasternal 
fossae.     The  choking  spell  may  occur  without  cause,  or  when  the  child 


DISEASES    OF    THE    LUNGS  515 

cries  from  pain  or  anger.  Hyperextension  of  the  head  or  dorsal  decubitus 
exaggerates  the  dyspnea.  This  would  explain  why  dyspnea  is  more 
marked  during  sleep  than  during  waking  hours"  (Crotti).  Finally,  there 
is  the  fulminant  type  in  which  death  occurs  suddenly  without  a  history 
of  previous  respiratory  trouble. 

In  the  absence  of  respiratory  symptoms  hyperplasia  of  the  thymus 
should  be  suspected  in  children  in  whom  the  body  fat  is  in  excess,  who 
are  anemic,  thick-skinned  and  who  have  facies  of  the  adenoid  type.  The 
superficial  lymph  nodes  will  often  be  found  to  be  unduly  enlarged,  the 
spleen  is  palpable  and  the  tonsillar  tissue  abundant.  A  blood  count  will 
frequently  show  an  excess  of  lymphocytes. 

Physical  Signs. — Inspection. — The  general  appearance  has  been 
referred  to.  In  many,  if  not  the  majority,  of  children  suffering  from 
an  enlarged  thymus  there  are  evidences  of  rickets.  Occasionally  there 
may  be  some  bulging  of  the  upper  part  of  the  sternum  and  in  extreme 
cases  a  tumor  may  be  seen  in  the  suprasternal  notch  during  forced 
expiration. 

Direct  inspection  of  the  upper  air  tract  will  reveal,  in  many  cases, 
hypertrophy  of  the  tonsils  and  the  presence  of  adenoids;  occasionally  the 
stenosis  of  the  trachea  can  be  seen. 

Palpation. — The  gland  may  be  felt  in  the  suprasternal  notch.  En- 
largement of  the  superficial  lymph  nodes  and  the  spleen  may  be  present. 

Percussion. — This  gives  the  most  important  information.  The  area 
of  dulness  is  triangular  in  shape  and  can  easily  be  determined  by  median 
percussion  over  the  manubrium.  The  dulness  extends  beyond  the  edges 
of  the  sternum  and  is  nearly  always  more  marked  to  the  left  than  the 
right.  On  the  left  side  the  dulness  can  be  elicited  in  the  first  and  second 
interspaces  and  occasionally  in  the  third;  on  the  right  in  the  first  inter- 
space and  less  frequently  in  the  second.  The  dulness  may  merge  into 
the  heart  dulness  below  (Fig.  309;  see  also  Figs.  Ill,  112,  113  and  114). 

Jacobi1  and  Boggs2  claim  that  the  thymus  is  movable  and  that  the 
mobility  of  the  organ  is  a  valuable  diagnostic  sign.  Jacobi  believes  that 
in  the  dorsal  decubitus  the  organ  falls  away  from  the  chest  wall.  He, 
therefore,  percusses  the  area  over  the  thymus  when  the  patient  is  lying 
on  the  back.  On  reversing  the  decubitus  and  percussing  from  under- 
neath, the  area  of  dulness  will  be  increased  if  the  thymus  is  enlarged  as 
the  gland  has  fallen  back  against  the  anterior  chest  wall.  Boggs,  from 
clinical  observations,  has  determined  that  the  gland  moves  up  and  down. 
It  can  be  made  to  shift  upward  by  hyperextension  of  the  head  in  the 
middle  line.  He  examines  the  patient  in  the  sitting  posture  and  de- 
termines the  lower  limit  of  dulness,  then  by  extending  the  head  the  dul- 
ness will  be  found  to  have  shifted  upward,  often  as  much  as  an  inter- 
space or  more.  Park  and  Maguire3  criticize  both  these  hypotheses  on 
the  ground  that  the  capsule  is  so  firmly  attached  to  surrounding  struc- 
ture as  to  preclude  movement.  They  suggest,  however,  that  the  thymus 
may  be  displaced  inside  its  own  capsule. 

While  some  assert  that  the  X-rays  fail  to  confirm  the  percussion 
area  of  dulness,  others  have  found  that  the  two  methods  agreed.  Hoch- 
singer  found  enlargement  of  the  thymus  by  both  percussion  and  radio- 

1  "Therapeutics  of  Infancy  and  Childhood,"  1908. 
-  Trans.  Assoc.  Am.  Phys.,  1911. 
3  Arch.  Int.  Med.,  September,  1912. 


516 


DISEASES    OF    THE    BKONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 


graphic  methods  in  26  out  of  58  children  examined.  Crotti  insists  that 
the  percussion  findings  should  always  be  checked  up  by  the  X-rays.  If 
enlargement  of  the  ttrymus  is  present,  a  more  or  less  triangular  shadow 
with  sharply  defined  edges  is  seen  in  the  superior  mediastinal  space.  It 
overlaps  the  normal  mediastinal  shadow  and  extends  upward  from  the 


Fig.  309. — Enlarged  thymus.      {Roentgenogram  by  Dr.  H.  K.  Pancoast.) 


base  of  the  heart.     In  some  cases,  it  is  superimposed  on  the  base  of  the 
heart  like  a  cap. 

Auscultation. — If  respiratory  disturbances  are  present  they  can 
usually  be  detected  without  the  aid  of  the  stethoscope  as  the  stridor  may 
be  audible  at  some  distance  from  the  body.  While  heard  all  over  the 
chest  the  stridor  is  more  intense  over  the  upper  part. 


DISEASES    OF    THE    LUNGS  517 

Diagnosis. — In  children  the  most  important  symptom  is  alteration  in 
the  character  of  the  breathing.  This  consists  of  a  persistent  stridor  both 
inspiratory  and  expiratory  but  most  marked  on  inspiration.  Children 
who  are  subject  to  this  type  of  breathing  may  suffer  from  paroxysmal 
suffocative  attacks  resembling  asthma.  In  some  instances  these  so- 
called  asthmatic  attacks  occur  at  intervals,  the  breathing  being  normal 
at  other  times. 

Congenital  stridor  may  be  due  also  to  malformation  of  the  vestibule 
of  the  larynx.  In  this  condition  the  difficulty  in  breathing  is  entirely 
inspiratory.  The  condition  may  be  recognized  by  direct  inspection 
with  the  laryngoscope  or  by  digital  examination. 

Enlarged  tuberculous  lymph  nodes  about  the  root  of  the  lung  may 
give  rise  to  stridor.  This  type  of  breathing  when  due  to  enlarged 
lymph  nodes  rarely  appears  before  the  fourth  month.  In  tuberculous 
adenitis  the  radiograph  gives  an  entirely  different  picture.  The  trouble 
is  seen  to  be  at  the  roots  of  the  lungs,  the  enlarged  lymph  nodes  show- 
ing as  distinct  isolated  shadows. 

In  adults  suffering  with  goitre,  especially  the  exophthalmic  type,  it  is 
important  to  have  in  mind  that  a  persistent  thymus  ma}r  be  present. 
The  differentiation  between  an  enlarged  thymus  and  an  intrathoracic 
goitre  may  present  some  difficulty.  In  goitre  there  is  an  up  and  down 
movement  synchronous  with  swallowing  which  may  be  detected  by  the 
fluoroscope.  This  up  and  down  movement  is  characteristic  of  goitre 
and  occurs  in  no  other  condition. 

Hernia  of  the  Lungs  (Pneumonoceie) 

This  is  a  rare  condition :  not  more  than  one  hundred  cases  have  been 
recorded  in  the  literature.  Two  groups  of  cases  are  recognized,  traumatic 
and  congenital. 

In  the  majority  of  instances  a  hernia  of  the  lung  is  traumatic  in  origin. 
When  an  open  wound  of  the  chest  occurs  it  is  followed,  almost  invariably, 
by  collapse  of  the  lung  and  the  formation  of  a  pneumothorax.  Occasion- 
ally, however,  and  under  circumstances  which  are  difficult  to  explain, 
a  portion  of  the  lung  protrudes  through  the  opening.  Makins1  in  an 
extensive  experience  with  chest  wounds,  observed  but  one  case  in  which 
this  accident  had  occurred.  The  condition  is  recognizable  at  a  glance. 
In  addition  to  open  wounds  the  chest  wall  may  be  weakened  by  a  severe 
strain,  a  blow,  or  a  crushing  accident.  Although  operations  on  the  chest 
wall,  at  times,  leave  a  point  of  weakened  resistance  through  which  the 
lung  tissue  may  bulge,  it  is  noteworthy  how  seldom  this  accident  occurs. 
The  hernia  may  develop  very  quickly  or  a  considerable  interval  may  in- 
tervene (consecutive  hernia). 

Congenital  hernia  is  the  result  of  some  defect  in  the  chest  wall.  As 
the  lungs  are  in  a  state  of  collapse  during  uterine  life  there  is  no  evidence 
of  the  trouble  until  some  weeks  or  months  after  birth.  Occasionally 
the  condition  does  not  manifest  itself  until  adult  life.  A  congenital 
hernia  is  most  apt  to  appear  in  the  lower  intercostal  spaces  near  the  junc- 
tion of  the  cartilage  with  the  rib. 

The  hernia  varies  greatly  in  size  ranging  from  one  the  size  of  an  almond 
to  a  clinched  fist.  The  hernia  may  be  enclosed  in  a  sac  formed  by  the 
1  "Surgical  Experiences  in  South  Africa,  1899-1900.*' 


518         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

pleura.  It  can  often  be  replaced  and  when  this  is  the  case  the  opening 
in  the  chest  wall  may  be  made  out  readily.  As  a  rule  there  are  no  symp- 
toms, but  in  some  instances,  during  the  initial  period  of  development, 
there  may  be  pain.  This  may  be  aggravated  by  deep  breathing  or 
coughing. 

The  tumor  consists  of  a  rounded  mass  which  is  soft,  elastic  and  crepi- 
tant. It  may  be  covered  with  smooth,  normal  skin  or,  as  in  the  case  of  a 
post-operative  hernia,  by  scar  tissue.  Coughing,  deep  breathing  or  change 
of  posture  may  cause  the  tumor  to  increase  in  size.  Over  the  tumor  the 
percussion  note  is  resonant  or  tympanitic,  the  breath  sounds  vesicular 
and  the  vocal  and  tactile  fremitus  are  increased.  In  some  instances  the 
hernia  may  appear  only  intermittently.  Strangulation,  although  rare, 
has  been  reported. 

The  following  conditions  may  be  confounded  with  a  pneumonocele: 
subcutaneous  emphysema,  empyema  necessitatis,  aneurism  or  tumor. 

Subcutaneous  emphysema  may  cause  a  localized  swelling  on  the  chest 
wall,  which  on  palpation  crepitates  and  on  percussion  gives  a  tympanitic 
note.  The  crepitation,  which  is  caused  by  the  movement  of  bubbles  of 
air  in  the  tissues,  may  not  only  be  felt  but  may  be  audible  as  well.  The 
condition  may  be  due  to  some  gas-producing  organism,  such  as  the  gas 
bacillus  of  Welch.  More  frequently  it  follows  a  punctured  wound, 
traumatic  or  operative.  It  is  not  uncommon,  for  instance,  after  paracen- 
tesis. Subcutaneous  emphysema  is  often  seen  in  the  lower  part  of  the 
neck  and  over  the  manubrium  as  the  result  of  trauma  or  a  violent  cough- 
ing paroxysm. 

In  empyema  necessitatis  the  external  tumor  may  increase  or  diminish 
in  size  during  coughing  or  forced  breathing.  The  differentiation,  as  in 
the  case  of  other  tumors  of  the  chest  wall,  depends  on  the  presence  or 
absence  of  crepitation  and  the  other  signs  commonly  found  in  hernia. 

Alterations  in  the  Extremities  Due  to  Chronic  Pulmonary 

Disease 

A  curious  feature  of  chronic  pulmonary  affections  is  the  frequency 
with  which  deformity  of  the  fingers,  toes  and  nails  occurs.  These  changes 
are  seen  also  in  congenital  heart  disease;  occasionally  there  is  no  demon- 
strable factor. 

THE  NAILS 

In  pulmonary  tuberculosis  abnormalities  involving  the  nails  are  ex- 
tremely common.  The  abnormality  to  be  noted  may  consist  of  a 
change  in  the  color,  in  the  contour  or  in  the  texture  of  the  nail.  In 
cases  of  advanced  phthisis,  the  nails  are  often  livid  and  may  be  slightly 
cyanotic  in  appearance.  In  the  early  stages  of  tuberculosis  the  nails 
may  be  of  an  exaggerated  pinkish  color,  closely  resembling  those  which 
have  been  stained  with  a  manicuring  paste,  or  they  may  have  a  slight 
violet  tinge.  In  either  case  these  changes  are  to  be  looked  upon  as  an 
evidence  of  serious  infection.  I  have  repeatedly  seen  these  changes  in 
the  nails  of  individuals  in  whom  the  disease  steadily  progressed  from  bad 
to  worse,  although  when  first  seen  the  amount  of  pulmonaiy  involve- 
ment spoke  for  a  favorable  prognosis. 

An  extremely  common  change,  especially  in  cases  of  tuberculosis,  is 


DISEASES    OF    THE    LUNGS  519 

curving  of  the  nails.  This  is  usually  an  exaggeration  of  the  normal  curve 
from  side  to  side  so  that  the  nail  appears  narrower  than  normal.  Not 
infrequently  the  lateral  curving  is  associated  with  a  turning  downward 
of  the  distal  portion  of  the  nail,  over  the  end  of  the  finger.  When  club- 
bing of  the  fingers  also  is  present  the  curving  downward  of  the  nail  over 
the  end  of  the  finger  is  usually  very  marked.  Among  3551  patients 
observed  at  the  Phipps  Institute  curving  of  the  nails  was  noted  in  1382  or 
38.9  per  cent. 

Longitudinal  and  transverse  striations  are  quite  common.  The  trans- 
verse striations  often  correspond  with  exacerbations  of  the  disease  and  are 
similar  to  those  occasionally  seen  after  an  acute  illness  of  any  kind. 

An  unusual  change,  occasionally  noted  in  those  suffering  from  some 
chronic  pulmonary  affection  is  the  so-called  "oyster-shell"  nail. 
Hirshberg1  first  called  attention  to  this  change.  Five  cases  have  been 
seen  at  the  Phipps  Institute.  The  nail  becomes  loosened  from  its  bed 
laterally  and  distally,  becomes  very  brittle  and  is  easily  broken.  It  is, 
also,  deformed  by  ridges  and  crater-like  depressions,  giving  it  the  appear- 
ance of  an  oyster  shell.     Both  the  fingers  and  toes  are  involved. 

CLUBBING  OF  THE   FINGERS  AND   TOES. 

This  curious  deformity  of  the  fingers  was  known  to  the  ancients  and 
was  in  later  times  referred  to  as  the  "Hippocratic  deformity  of  the 
fingers."  The  toes  are  often  involved  but  never  to  the  same  extent  as 
the  fingers.  Occasionally  the  nose  assumes  a  bulbous  or  clubbed 
appearance. 

Clubbing  of  the  fingers  is  very  common  in  cases  of  pulmonary  tuber- 
culosis. It  is  seen  in  its  most  exaggerated  form,  however,  in-  bronchiec- 
tasis, empyema  and  congenital  heart  disease.  In  the  ordinary  chronic 
type  of  pulmonary  tuberculosis,  the  clubbing  is  never  extreme;  when  it  is 
one  can  be  reasonably  certain  that  the  tuberculosis  is  associated  with 
marked  fibrosis  of  the  lung  and  dilatation  of  the  bronchi.  In  a  group  of 
potters  seen  at  the  White  Haven  Sanatorium  extreme  clubbing  of  the 
fingers  was  noted  in  10  of  the  21  reported.2  In  these  cases  the  primary 
trouble  was  a  pulmonary  fibrosis  associated  with  dilatation  of  the  bronchi, 
resulting  from  the  inhalation  of  inorganic  dust.  Later  a  tuberculous 
infection  was  superadded.  Among  3551  cases  of  tuberculosis  seen  at  the 
Phipps  Institute  varying  degrees  of  clubbing  of  the  fingers  was  noted  in 
772  or  21.7  per  cent.  In  extreme  examples  of  the  condition  the  associa- 
tion with  bronchiectasis  is  so  frequent  as  to  be  of  considerable  diagnostic 
value  and  the  same  is  true  of  the  association  of  marked  clubbing  and 
cyanosis  with  congenital  heart  disease  (see  Fig.  1) . 

In  the  vast  majority  of  cases  the  development  of  the  clubbing  is 
insidious  and  slow  and  usually  passes  unnoticed  by  the  patient.  Rarely 
it  develops  quickly.  West3  records  two  cases  in  which  the  clubbing 
developed  in  two  and  four  weeks  respectively  and  Godlee4  mentions  a  case 
in  which  well-marked  clubbing  appeared  in  two  months.  Aside  from  the 
deformity  -there  are  no  symptoms  although  occasionally  pain  is  com- 
plained of  in  rapidly  developing  cases.     Once  established  the  deformity 

1  Am.  Jour.  D?rmalology,  August,  1911. 

2  Am.  Jour.  Public  Health,  1914,  vol.  iv,  No.  9. 

3  Trans.  Clin.  Soc,  vol.  xxx,  1897. 

4  Fowler  and  Godlee:  "Diseases  of  the  Lungs,"  1898. 


520  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

is  permanent  although   some  improvement  has  been  noted  after  the 
drainage  of  an  empyema. 

In  simple  clubbing  the  enlargement  is,  for  the  most  part,  due  to  a 
hyperplasia  of  the  soft  parts,  principally  fat.  Two  clubbed  fingers  (shown 
in  Fig.  310)  which  I  had  removed  at  autopsy  and  placed  in  Kaiserling's 
fluid  both  lost  the  deformity;  Fowler  had  a  similar  experience  with  a 
clubbed  finger  preserved  in  alcohol.  Since  the  introduction  of  the 
X-rays  it  has  been  shown  that  in  many  cases  there  is  also  some  increase  in 
the  bony  parts.  Usually  the  change  is  limited  to  the  terminal  phalanx 
but  there  may  be  present  also  some  periosteal  proliferation  of  the,  long 
bones.  Locke1  states  that  the  Roentgen-ray  examination  of  39  cases 
of  simple  clubbing  showed  alterations  of  varying  degree  in  the  ungual 


Fig.  310. — Simple  clubbing. 

phalanges  in  5  cases  and  periosteal  proliferation  of  the  long  bones  in  12. 
The  change  noted  in  the  terminal  phalanges  consists  of  a  proliferation 
of  the  distal  half,  usually  giving  a  distinct  chestnut-burr  appearance 
(Fig.  311),  and  occasionally  immense  burr-like  processes  are  seen. 

The  affection  is  almost  always  bilateral  and  symmetrical  and  is  said 
to  take  place  first  in  the  thumb  and  forefinger ;  later  the  other  fingers  also 
become  clubbed.  A  few  cases  have  been  reported  in  which  the  deformity 
was  unilateral  and  associated  with  an  aneurism  of  the  subclavian  artery. 
Such  cases  are  not  instances  of  true  clubbing  but  are  to  be  regarded  as  a 
form  of  edema  due  to  interference  with  the  circulation.  The  deformity 
consists  of  enlargement  and  thickening  of  the  digital  pulp  of  the  ungual 
phalanx  associated  with  curving  downward  of  the  end  of  the  nail.  This 
type  of  nail  is  sometimes  referred  to  the  " parrot-beak"  nail.  Owing  to 
the  bulbous  appearance  of  the  terminal  phalanges,  fingers  so  deformed 
have  been  likened  to  the  end  of  a  club  or  a  drumstick;  Trousseau  com- 
pared the  enlargement  to  the  head  of  a  serpent  (Fig.  312).  The  skin 
1  Arch.  Int.  Med.,  May,  1915,  Part  I. 


DISEASES    OF    THE    LUNGS 


521 


Fig.  311. — Radiograph  of  clubbed  fingers  in  hypertrophi  cpulmonary  osteo-arthropathy 
"  Burring,"  of  terminal  phalanges. 


Fig.   312. — Clubbing  in  hypertrophic  pulmonary  osteo-arthropathy 


522         DISEASES    OP    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

over  the  bulbous  portion  of  the  finger  is  usually  shiny  and  stretched  in 
appearance.  In  the  rapidly  developing  type  the  swelling  of  the  soft 
parts  is  extreme,  the  nail  bed  is  deeply  injected  and  swollen  and  the  nails 
are  red.  This  is  especially  apt  to  occur  in  cases  of  empyema;  the  most 
marked  example  which  has  come  to  my  notice  was  in  a  case  of  recurrent 
sarcoma  with  extensive  metastasis  to  the  lungs  (see  Fig.  3).  In  the 
slowly  developing  type  the  color  of  the  skin  and  nail  may  be  of  a  deeper 
pink  than  normal  or  it  may  be  dusky  and  livid.  When  the  clubbing  is 
associated  with  congenital  heart  disease,  both  the  nails  and  fingers  are 
markedly  cyanotic  (see  Fig.  1). 

"When  true  clubbing  of  the  fingers  is  present,  if  the  observer  places 
one  of  his  fingers  upon  the  upper  edge  of  the  nail  at  its  free  margin,  i.e., 
the  distal  end,  and  his  thumb  upon  the  under  surface  of  the  clubbed  finger, 
and  presses  downward,  the  hard  margin  of  the  root  of  the  nail  can  be 
distinctly  felt  if  another  finger  is  applied  over  it"  (Fowler). 

HYPERTROPHIC  PULMONARY  OSTEO-ARTHROPATHY 

Attention  was  first  called  to  this  remarkable  deformity  by  Bamberger1 
and  Marie.2  The  name  of  the  latter  has  been  especially  associated  with  the 
condition.  Since  the  appearance  of  these  original  papers  numerous  studies 
of  collected  cases  have  been  made.  Among  these  may  be  mentioned  the 
papers  by  Walters,3  Thayer,4  Janeway,5  Wynn,6  Ebstein,7  and  Alexander.8 
The  most  recent  and  the  most  complete  study  is  that  by  Locke.9 

The  original  name  has  been  subject  to  various  changes  and  modifica- 
tions. The  following  terms  have  been  suggested:  Secondary  hyper- 
trophic osteo-arthropathy,  hyperplastic  osteo-arthropathy,  secondary 
hyperplastic  ostitis,  toxigenic  ossifying  osteo-periostitis,  tuberculous 
polyarthritis.  Next  to  the  original  name,  secondary  hypertrophic 
osteo-arthropathy  has  been  most  used.  The  only  advantage  it  possesses 
is,  that  it  gets  over  the  difficulty  that,  in  some  cases,  no  pulmonary  lesion 
has  been  found;  on  the  other  hand,  it  fails  to  cover  those  cases  in  which 
the  disease  is  apparently  primary.  It  seems  to  me  that  Marie's  original 
name  had  best  be  retained  as  the  others  are  just  as  cumbersome,  and  do 
not  express  any  more  clearly  the  conditions  present. 

Etiology. — Males  are  affected  more  frequently  than  females,  the 
proportion  being  nearly  8  to  1.  With  two  or  three  exceptions  all  the 
cases  reported  have  occurred  in  the  white  race.  No  age  period  is  exempt 
but  the  vast  majority  of  cases  occur  in  the  third  and  fourth  decades.  The 
greater  liability7"  to  pulmonary  affections  during  the  third  and  fourth 
decades  doubtless  influences  the  osteo-arthropathic  change  rather  than 
the  condition  of  the  bones. 

The  condition  is  almost  invariably  secondary  to  some  obvious 
primary  disease,  usually  of  the  lungs  or  bronchi.     Locke  has  been  able 

1  Wien.  Klin.  Woch.,  1889,  ii,  225;  Zeit.  f.  Klin.  Med.,  1891,  viii,  193. 

2  Revue  de  vied.  1890,  x,  1. 

3  St.  Thomas  Hospital  Report,  1895. 

4  Phila.  Med.  Jour.,  1898. 

5  Am.  Jour.  Med.  Sc,  January,  1903. 

6  Birmingham  Med.  Review,  1904. 

7  Deut.  Arch.  f.  Klin.  Med.  [Festschrift],  1906,  lxxxix,  68. 

8  St.  Bartholomew  Hospital  Report,  xlii,  1906. 

9  Arch.  Int.  Med.,  May,  1915,  Part  I. 


DISEASES    OF    THE    LUNGS  523 

to  find  but  5  cases  which  offer  any  definite  positive  evidences  of  the 
existence  of  primary  origin.  From  a  study  of  the  reported  cases  Locke 
found  139  which  meet  all  the  requirements;  to  this  number  he  adds  5 
personal  observations;  making  144  in  all.  .1  believe  that  this  does  not 
by  any  means  represent  the  true  proportion.  Doubtless  many  cases 
have  been  recognized  and  not  reported,  and  probably  a  still  larger 
number  have  gone  unrecognized  or  have  been  looked  upon  as  cases  of 
ordinary  clubbing  of  the  fingers.  Within  the  past  three  years,  I  have  seen 
three  typical  cases. 

The  role  played  by  chronic  respiratory  affections  is  well  recognized. 
Of  the  144  cases  reported  by  Locke  113  were  associated  with  disease  of 
the  respiratory  tract;  6  with  disease  of  the  circulatory  tract;  13  with  dis- 
ease of  the  alimentary  tract,  of  which  6  occurred  with  hypertrophic  biliary 
cirrhosis;  7  were  associated  with  miscellaneous  conditions  and  5  were 
apparently  primary.  Of  the  individual  diseases  pulmonary  tuberculosis 
heads  the  list  with  30  or  20  per  cent.;  bronchiectasis  28  or  19  per  cent.; 
malignant  disease  10  or  7  per  cent,  and  empyema  8  or  5  per  cent.  Al- 
though bronchiectasis  stands  second  I  am  inclined  to  believe  it  is  by  far 
the  most  important  disease  as  many  of  the  cases  of  chronic  tuberculosis 
are  associated  with  marked  fibrosis  and  dilatation  of  the  bronchi.  Why 
these  various  conditions  should  be  associated  with  osteo-arthropathic 
changes  is  not  at  all  clear.  Various  hypotheses  have  been  advanced, 
the  most  probable  of  which  seems  to  be  that  the  changes  are  in  some 
way  dependent  on  toxic  absorption;  this  was  Marie's  idea  and  also 
Bamberger's.  That  it  is  the  most  reasonable  explanation  is  to  be  in- 
ferred from  the  fact  that  extreme  clubbing  of  the  fingers  is  almost  ex- 
clusively associated  with  bronchiectatic  cavities  in  the  lower  lobes.  In 
this  situation  the  drainage  is  poor  and  the  secretions  stagnate.  When 
the  dilated  bronchi  are  confined  to  the  apex  of  the  lung  clubbing  of  the 
fingers  is  rarely  present  as  the  drainage  is  good. 

Morbid  Anatomy.- — The  changes  consist  primarily  in  a  slowly  pro- 
gressive, ossifying  periostitis  beginning  usually  in  the  distal  ends  of  the 
diaphyses  of  the  bones  of  the  forearm  and  lower  legs,  later  involving  also 
the  other  bones  of  the  limbs  and  even  in  some  cases  nearly  all  the  re- 
maining bones  of  the  skeleton.  The  periosteum  is  thickened,  more 
vascular  than  normal,  and  shows  subperiosteal  deposit  of  new  bone.  At 
first  the  new  bone  is  sharply  differentiated  from  the  old  shaft  but  at  a 
later  period  the  two  become  indistinguishable.  The  cortex  of  the  bones 
shows  sclerosis  and  thickening  with  diminution  of  the  medullary  cavity. 
The  medulla  is  embryonic  in  character,  with  a  tendency  to  fatty  degenera- 
tion in  its  central  part.  Locke  states  that  in  the  most  extreme  cases  there 
remains  scarcely  any  of  the  appearances  of  the  original  bone  but  instead 
the  osseous  tissue  appears  very  thin,  and  of  a  coarse,  irregular  structure. 
In  general  such  cases  resemble  osteitis  deformans  but  without  the  curving 
or  deformity,  except  in  outline,  which  is  characteristic  of  the  latter  dis- 
ease. In  addition  to  the  subperiosteal  new  bone  osteophyte  growths 
are  often  present  (Fig.  313).  Hall1  has  reported  a  case  in  which  the 
affected  bones  were  characterized  by  softness  of  texture,  the  post- 
mortem knife  dividing  them  easily.  The  evolution  of  the  bony  changes 
can  easily  be  followed  by  means  of  frequent  examinations  with  the  Roent- 
gen rays. 

1  Edinburgh  Med.  Jour.,  New  Series,  vol.  xviii,  1905. 


524  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

In  addition  to  the  changes  in  the  bones  the  joints  show  erosions  of 
the  articular  cartilages,  periarticular  thickening,  and  thickening  of  the 
synovial  membrane  with  an  excessive  amount  of  fluid.  The  soft  parts 
are  also  increased  in  size  principally  as  the  result  of  a  hyperplasia  of  the 
fatty  tissue.  Associated  pathological  changes  have  been  described 
in  individual  cases  but  none  of  them  are  constant  and  must  be  looked 
upon  either  as  coincidences,  or  in  some  way  related  to  the  primary  disease. 


Fig.  313.— Radiograph  of  elbow-joint  showing  spicula  of  bone  at  upper  end  of  ulna. 
Shafts  of  radius  and  ulna  also  show  a  roughened  and  uneven  appearance  similar  to  chronic 
periostitis. 

Symptoms. — The  symptoms  of  hypertrophic  pulmonary  osteo- 
arthropathy are  almost  entirely  objective.  In  rapidly  developing  cases 
pain  in  the  hands  is  sometimes  complained  of  and  there  may  be  present 
also  pain  and  stiffness  in  the  affected  joints.  These  symptoms  may  occur 
during  an  acute  exacerbation  of  a  chronic  case.  In  the  great  majority 
of  cases  the  disease  develops  slowly  and  the  patient  is  often  unconscious 


DISEASES    OF   THE    LUNGS  525 

of  the  changes  until  attention  has  been  drawn  to  it.  Briefly  stated  the 
changes  consist  in  a  symmetrical  enlargement  of  the  hands,  most  marked 
in  the  finger  tips,  which  are  enlarged  and  bulbous,  the  so-called  drumstick 
fingers.  The  nails  are  sharply  curved  downward,  and  resemble  a  parrot's 
beak.  Enlargement  of  the  lower  part  of  the  forearm  accompanies  this 
change  in  the  hands.  The  enlargement  is  clue  partly  to  the  formation  of 
new  bone  and  partly  to  hypertrophy  of  the  soft  tissues.  Analogous 
changes  take  place  in  the  feet  and  legs.  Locke  has  emphasized  the  fact 
that  X-ray  studies  have  shown  that  while  the  bones  of  the  forearms  and 
legs  are  most  frequently  involved  the  bones  in  any  part  of  the  body  may 
be  enlarged.     Effusions  into  the  joints  are  common,  the  joints  most 


Fig.  314. — Enlargement  of  both  legs  in  a  case  of  hypertrophic  pulmonary  osteo-arthropathy 
with  large  effusion  in  left  knee-joint. 

frequently  affected  being  those  nearest  the  bony  changes,  as  the  ankle, 
knee,  wrist  or  elbow.  Rarely  the  hip  and  shoulder  joints  are  involved. 
The  symmetrical  distribution  of  the  lesion  is  characteristic  but  occasion- 
ally one  side  is  more  involved  than  the  other.  This  occurred  in  a  case 
I1  reported  some  years  ago  in  which  the  changes  in  the  hands  and  fore- 
arms were  symmetrical  but  in  the  lower  extremities  one  side  was  much 
larger  than  the  other  (Fig.  314). 

Pain  is  rarely  complained  of  but  the  greatly  increased  size  of  the  hands 
may  interfere  with  the  finer  movements,  such  as  needle  work  or  writing. 
Sweating  of  the  palms  of  the  hands  and  soles  of  the  feet  is  common. 

1  Penna.  Med.  Jour.,  August,  1907. 


526         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Involvement  of  the  joints  may  produce  stiffness,  pain  or  disturbance,  of 
function.  Spinal  curvature  (kyphosis  or  scoliosis)  is  not  infrequently 
present  and  there  may  also  be  clubbing  and  redness  of  the  end  of  the  nose. 
Aside  from  the  changes  in  the  extremities  there  are  no  other  symptoms. 

In  speaking  of  simple  clubbing  it  was  pointed  out  that  the  deformity 
occasionally  disappeared,  as  for  instance,  following  the  draining  of  an 
empyema.  In  such  cases  the  enlargement  is  confined  to  the  soft  tissues. 
In  hypertrophic  pulmonary  osteo-arthropathy  the  bony  changes  are  per- 
manent. These  changes  may  occur  very  rapidly,  or  they  may  develop 
slowly  or,  as  is  probably  true  of  most  of  the  cases,  the  changes  pursue  an 
irregular  clinical  course  which  is  subject  to  exacerbations  and  remissions 
depending  on  an  increased  activity  or  improvement  of  the  primary 
condition. 

Relation  of  Simple  Clubbing  to  Hypertrophic  Pulmonary  Osteo-arthro- 
pathy.— Some  years  ago  I  expressed  the  opinion  that  simple  clubbing  was 
to  be  looked  upon  as  an  incipient  or  arrested  stage  of  hypertrophic 
pulmonary  osteo-arthropathy,  a  view  which  Locke  supports.  There  are 
several  reasons  for  this:  (1)  Both  simple  clubbing  and  hypertrophic 
osteo-arthropathy  are  associated  with  the  same  general  group  of  diseases; 
(2)  clubbing  of  the  fingers  is  one  of  the  characteristic  features  of  hyper- 
trophic osteo-arthropathy;  (3)  the  clubbing  which  occurs  in  the  hippo- 
cratic  fingers  is  identical  with  that  occurring  in  osteo-arthropathy,  except 
perhaps  in  the  degree  of  development;  (4)  osseous  changes  sometimes 
occur  in  simple  clubbing  which  are  precisely  the  same  as  those  seen  in 
hypertrophic  osteo-arthropathy;  12  out  of  39  cases  of  simple  clubbing 
studied  by  Locke  showed  bony  changes. 

Diagnosis. — The  diagnosis  is,  as  a  rule,  easjr  and  rests  on  the  char- 
acteristic changes  in  the  extremities  associated  most  frequently  with 
disease  of  the  lungs.  The  extent  of  the  change  is  easily  determined  by 
Roentgen-ray  studies.  The  condition  has  a  superficial  resemblance  to 
acromegaly.  The  latter  is  a  primary  disease  due  to  alterations  in  the 
pituitary  body,  and  is  ultimately  fatal.  While  it  causes  enlargement  of 
the  feet  and  hands,  the  nails  are  not  changed,  and  it  involves  the  whole 
part  symmetrically;  joint  effusions  are  rare.  Furthermore,  in  acromeg- 
aly, the  face,  lower  jaw,  tongue  and  genitals  are  enlarged  as  are  also 
the  cartilages  of  the  ear,  nose,  eyelids  and  epiglottis  (see  Fig.  3) . 


CHAPTER  XXIII 
DISEASES  OF  THE  PLEURA 

PLEURISY 

Etiology. — Inflammation  of  the  pleura  is  a  very  common  affection, 
which  may  manifest  itself  either  as  a  primary  or  a  secondary  process. 
In  the  great  majority  of  instances  pleuritis  is  secondary  to  some  pre- 
existing condition. 

Until  within  recent  years  primary  pleurisy  was  looked  upon  as  of 
frequent  occurrence.  This  was  clue  to  the  fact  that  a  large  number  of 
instances  were  observed  in  individuals  who  were  apparently  healthy, 
and  in  whom  the  attack  followed  exposure  to  cold,  the  so-called  pleurisy 
a  frig  ore.  While  a  primary  pleurisy  can  be  produced  by  exposure  to 
cold,  it  is  now  known,  as  I  shall  show  later,  that  the  majority  of  these 
so-called  idiopathic  cases  are  in  reality  tuberculous  in  nature. 

Traumatic  injury  of  the  chest  wall  is  the  only  other  condition  which 
is  apt  to  produce  a  primary  inflammation  of  the  pleura. 

Secondary  pleurisy  as  a  rule,  originates  in  one  of  two  ways:  (1) 
By  extension  of  an  inflammatory  process,  involving  the  lungs,  pericardium 
or  mediastinum,  and  occasionally  the  liver;  (2)  the  pleura  may  be  infected 
by  way  of  the  blood  stream  in  cases  of  general  septicemia.  Pleurisy  also 
occurs  in  certain  of  the  chronic  diseases  such  as  nephritis  and  gout. 

By  far  the  commonest  source  of  pleural  inflammation  is  pulmonary 
disease.  There  are  very  few  instances  of  disease  of  the  lung,  either  acute 
or  chronic,  in  which  the  pleura  is  not  secondarily  involved.  Thus  we 
see  pleurisy  associated  with  croupous  pneumonia,  broncho-pneumonia, 
pulmonary  abscess  and  gangrene,  hemorrhagic  infarction  and  emboli, 
the  mycotic  infections,  and  most  important  of  all  pulmonary  tuberculosis. 

Inasmuch  as  tuberculosis  is  by  far  the  most  frequent  pulmonary 
infection  encountered  this  disease  overshadows  all  others  as  an  exciting 
cause  of  pleurisy.  I  have  already  alluded  to  the  fact  that  at  one  time 
idiopathic  pleurisy  was  considered  to  be  of  frequent  occurrence.  But 
the  intensive  studies  which  have  been  made  of  tuberculosis  in  all  its 
manifestations,  during  the  past  decade,  have  shown  conclusively  that  the 
great  majority  of  all  cases  of  apparently  primary  pleurisy  are  tuberculous. 
It  must  never  be  lost  sight  of  that  primary  pleurisy  is  relatively  infre- 
quent, and  that  in  the  absence  of  a  demonstrable  lesion  which  might 
cause  it,  a  tuberculous  origin  is  to  be  thought  of  whether  exposure  to 
cold  has  occurred  or  not.  Hemoptysis  or  an  attack  of  pleurisy  are  two 
of  the  ways  in  which  a  pulmonary  tuberculosis  may  suddenly  manifest 
itself  in  an  individual  who  is  apparently  healthy.  In  most  cases  a  readily 
demonstrable  pulmonary  lesion  is  present;  in  others  the  lungs  seem  to 
be  normal.  In  eve^  instance,  however,  the  patient  should  be  given  the 
benefit  of  the  doubt,  and  warned  as  to  the  possible  significance  of  the 
pleurisy.     In  the  case  of  a  serofibrinous  effusion,  especially  one  which 

527 


528  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

has  developed  insidiously  and  with  no  symptoms,  the  probability  of  its 
being  tuberculous  in  origin  is  almost  a  certainty. 

The  argument  is  frequently  used  that  many  individuals  who  have  had 
pleurisy  with  or  without  effusion,  have  never  developed  clinical  tubercu- 
losis. Of  this  there  is  no  doubt.  On  the  other  hand,  many  more  such 
patients  actually  do  have  tuberculosis  or  subsequently  develop  it.  The 
records  of  the  Phipps  Institute  show  that  of  5895  patients  in  whom  a 
diagnosis  of  tuberculosis  was  made,  23.8  per  cent,  gave  an  antecedent 
history  of  pleurisy. 

So  long  as  there  is  doubt  as  to  which  are  really  primary  and  which  are 
secondary  to  a  latent  tuberculosis  it  is  unwise  to  assure  the  patient  that 
the  trouble  is  trivial  in  nature. 

Morbid  Anatomy. — Inflammatory  changes  involving  the  pleura  may 
be  unilateral  or  bilateral  and  may  be  limited  to  a  small  circumscribed 
area,  or  involve  all  of  one  side.  Any  part  of  the  pleural  surface  may  be 
the  seat  of  the  inflammatory  process.  Post-mortem  experience  shows 
that  the  pleural  covering  of  the  apices  of  the  lungs,  especiallj-  posteriorly, 
is  most  frequently  involved,  although  there  is  little  evidence  of  this  during 
life  (see  Fig.  237).  Probably  the  next  most  -common  site  is  the  lower 
part  of  the  chest  anteriorly  and  laterally.  It  is  a  matter  of  clinical  ob- 
servation that  pain  and  friction  rubs  are  more  frequently  encountered  in 
these  areas  than  elsewhere.  I  have  already  pointed  out  the  probable 
tuberculous  origin  of  many  of  these  cases.  White1  in  an  analysis  of  197 
autopsied  cases  of  tuberculosis  found  that  a  favorite  site  for  old  pleuritic 
adhesions  was  along  the  course  of  the  third,  fourth  and  fifth  ribs  an- 
teriorly, from  the  parasternal  or  mid-clavicular  line  to  the  mid-axillary 
line.  In  tuberculosis  cases  it  happens  not  infrequently,  that  with  disease 
at  one  apex  a  dry  or  fibrinous  pleurisy  will  develop  over  the  base  of  the 
opposite  lung.  In  rare  instances  the  pain  is  manifest  on  the  side  not 
affected.  Finally,  it  should  be  mentioned  that  the  inflammation  may  be 
limited  in  part  or  entirely  to  the  diaphragmatic  surface. 

The  exciting  cause  of  the  inflammation,  in  the  great  majority  of  cases, 
is  either  the  tubercle  bacillus,  the  pneumococcus  or  the  streptococcus. 
The  intensity  of  the  inflammation  depends,  to  some  extent,  on  the  char- 
acter of  the  infection.  In  the  very  severe  and  acute  attacks  any  one  of 
the  above-mentioned  organisms  may  be  the  cause,  but  if  the  attack  is 
insidious  and  attended  with  little  or  no  pain  the  tubercle  bacillus  is  in  all 
probability  the  exciting  cause. 

In  fibrinous  or  plastic  'pleurisy  the  surfaces,  first  of  the  visceral  and 
then  of  the  parietal  layer,  lose  their  luster  and  polished  appearance,  be- 
come congested  and  dull  and  finally  show  a  fibrinous  exudate  which  in 
pneumonic  pleurisies  is  usually  very  widespread. 

The  fibrinous  form  may  terminate  as  such  leaving  no  evidence  of 
having  existed.  More  commonly  the  fibrinous  deposit  undergoes  pro- 
liferative changes  which  produce  adhesions  between  the  visceral  and 
parietal  layers.  The  adhesions  may  be  extensive  on  both  sides  and  may 
be  dense  in  some  places  and  fragile  and  easily  broken  up  in  others. 
Complete  obliteration  of  the  pleural  sac  is  relatively  common.  In  such 
cases  the  pleural  surfaces  are  firmly  united,  attaching  the  lung  to  the 
chest  wall  and  diaphragm  throughout.  Often  the  lung  is  firmly  bound 
down  and  cannot  be  removed  from  the  chest  except  by  cutting  it  free. 
1  Phipps  Institute  Report,  1907. 


DISEASES    OF   THE    PLEURA 


529 


Chronic  obliterative  pleurisy  may  originate  from  an  acute  pneumonic 
pleurisy  or  pleurisy  of  other  bacterial  origin.  In  tuberculosis  the 
pleural  thickening  is  rarely  uniform  throughout.  Usually  it  is  dense  at 
the  apices  while  in  the  inferior  parts  the  adhesions  are  lace-like  in  char- 
acter.    Complete  obliteration  of  both  pleural  sacs  is  sometimes  noted. 

In  a  certain  proportion  of  cases  the  fibrinous  exudate  becomes  ex- 
cessive in  amount  and  in  addition  there  is  an  exudate  from  the  capillaries 


Fig.  315. — Section  through  the  right  sterno-clavicular  articulation,  showing  pneu- 
monia (gray  hepatization)  with  a  moderate  amount  of  serous  exudate  in  the  upper  and 
lower  margins  of  the  pleura.      (Pirogoff.) 

of  the  pleura,  constituting  what  is  known  as  serous  or  serofibrinous 
pleurisy.  The  quantity  of  fluid  varies  from  that  which  barely  can  be 
recognized  by  physical  signs  to  an  amount  that  nearly  fills  the  pleural 
sac.  If  the  primary  inflammation  is  severe  in  character  the  serofibrinous 
exudate  may  be  poured  out  rapidly  and  evidences  of  an  effusion  be  mani- 
fest within  a  few  days  from  the  onset  of  the  pain.  In  other  instances  the 
fluid  accumulates  gradually  and  is  unsuspected  until  it  has  reached  a 
large  amount.  Although  not  a  common  occurrence  a  serous  effusion  is 
occasionally  encysted  (see  Figs.  315  and  316). 

34 


530 


DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 


The  fluid  in  the  serofibrinous  form  is  yellowish  or  of  a  faintly  green 
tint  containing  flakes  or  coagulated  masses  of  fibrin.  In  some  instances 
the  fibrin  may  be  so  abundant  that  the  effusion  presents  a  gelatinous 
appearance.  Microscopically  leukocytes  and  a  few  blood  cells  are  noted. 
An  excess  of  lymphocytes  points  to  a  tuberculous  origin  of  the  disease. 
For  details  as  to  the  bacteriology  of  pleural  exudates  the  reader  is  referred 
to  any  of  the  standard  text-books  on  laboratory  diagnosis. 


Fig.  316. — Pleural  effusion  (probably  localized  posteriorly).  Fluoroscopic  examination 
of  chest:  The  right  diaphragm  was  almost  fixed,  scarcely  any  movement  being  perceptible. 
Almost  the  entire  right  side  of  the  chest  was  very  much  obscured  by  what  appeared  to  be  a 
localized  effusion.  This  extended  fro-m  the  outer  corner  of  the  diaphragm  upward  to  the 
apex,  but  did  not  extend  to  the  heart  and  aortic  shadows,  over  one-quarter  to  three- 
quarters  of  an  inch  of  clear  space  being  seen  between  the  opaque  region  and  the  aortic  and 
heart  shadows.  The  shading  was  not  so  dense  as  to  hide  the  ribs  and  diaphragm.  On 
lateral  inspection  a  clear  space  could  be  seen  in  front  of  the  chest,  which  would  indicate  that 
the  possible  effusion  was  posterior.      (Dr.  D.  R.  Bow  en.) 


Artificial  pneumothorax  in  the  treatment  of  pulmonary  tuberculosis 
is  very  frequently  followed  by  an  effusion  which  may  require  frequent 
tappings.  Occasionally  the  effusion  becomes  purulent;  two  such  acci- 
dents occurred  among  the  cases  treated  at  the  Phipps  Institute. 

Purulent  effusion  may  be  such  from  the  onset  and  this  is  especially 
true  when  the  offending  organism  is  the  streptococcus.     It  should  be 


DISEASES    OP   THE    PLEURA  531 

borne  in  mind  that  in  pneumococcus  pleurisies  the  exudate  is  usually 
purulent.  More  frequently,  however,  the  effusion  is  primarily  serous 
in  character,  or  possibly  turbid  in  appearance.  The  subject  of  empyema 
will  be  dealt  with  under  a  separate  heading. 

At  times  the  effusion  is  hemorrhagic  in  character.  Hemorrhagic 
effusions  and  hemothorax  are  also  considered  under  separate  headings. 

Pressure  Effects. — The  degree  of  pressure  which  will  be  exerted  on  the 
lung  of  the  affected  side  and  adjacent  viscera  will  depend  on  the  size  of 
the  effusion.  Even  with  very  small  collections  of  fluid  the  base  of  the 
lung  in  immediate  contact. with  the  fluid  becomes  atelectatic.  As  the 
fluid  accumulates  the  lung  is  more  and  more  compressed  until,  in  extreme 
cases,  it  has  been  reduced  to  a  small,  elongated  and  flattened  mass 
occupying  the  upper  and  posterior  part  of  the  chest  along  the  spine  (see 
Fig.  325).  The  lung  is  generally  airless  and  tough  and  leathery  to  the 
touch.  If  the  effusion  occupies  the  right  side  of  the  chest  the  heart  is 
displaced  to  the  left  beyond  its  normal  position,  and  the  liver  is  forced 
downward  by  the  flattening  of  the  diaphragm  (see  Fig.  327).  If  the 
effusion  is  left-sided  the  heart  is  displaced  to  the  right;  in  extreme  cases 
pulsation  may  be  seen  in  the  fourth  or  fifth  interspace  to  the  right  of  the 
sternum.  The  diaphragm  is  also  flattened  on  this  side  forcing  downward 
the  spleen,  stomach  and  left  lobe  of  the  liver  (see  Fig.  103) . 

If  the  effusion  develops  rapidly  dyspnea  may  occur,  because  the 
opposite  lung  has  not  had  time  to  adjust  itself  to  the  increased  work 
thrust  upon  it.  In  slowly  developing  effusions  considerable  compensa- 
tory emphysema  will  be  noted  in  the  unaffected  lung.  Leon,  LePlay 
and  Mantoux1  have  shown  experimentally  that  after  establishing  a 
complete  unilateral  thorax  in  dogs  a  partially  progressive  increase  in 
the  thorax  is  established  on  the  opposite  side.  In  order  to  determine 
how  small  a  portion  of  functionating  lung  was  compatible  with  life  they 
found  that  one-sixth  of  the  total  lung  capacity  was  sufficient  to  maintain 
life  under  ordinary  conditions.  This  shows  the  extent  to  which  the  lungs 
may  be  functionally  incapacitated  either  as  the  result  of  pleural  effusion 
or  extensive  tuberculous  disease,  without  producing  death. 

From  the  foregoing  description  it  will  be  seen  that  the  various  stages 
have  a  fixed  sequence,  a  fact  of  the  greatest  importance,  because  they 
correspond  in  a  striking  manner  to  the  physical  signs  and  even  the  symp- 
toms of  the  disease.  To  recapitulate:  (1)  The  dry  stage  in  which  the 
inflamed  pleural  surface  becomes  vascular  and  loses  its  moist  and 
polished  appearance.  (2)  The  fibrinous  stage  in  which  the  affected  area 
becomes  coated  with  flakes  of  lymph.  It  is,  of  course,  understood  that  the 
process  in  the  majority  of  instances  does  not  progress  beyond  the  first 
or  second  stages.  Chronic  obliterative  pleurisy  is  probably  a  sequel  of 
a  widespread  fibrinous  deposit  which  undergoes  connective  tissue  changes, 
and  firmly  unites  the  two  layers  of  the  pleura.  (3)  The  stage  of  effusion 
which  may  be  serous,  serofibrinous,  purulent  or  hemorrhagic,  and  which 
appears  first  at  the  base  of  the  chest.  As  the  accumulation  of  fluid 
increases  pressure  effects  manifest  themselves  by  compression  of  the 
lung  and  displacement  of  the  viscera.  (4)  The  stage  of  absorption  and 
reexpansion  of  the  lung.  Whether  the  lung  will  return  to  its  normal  state 
will  depend  largely  on  the  length  of  time  it  has  been  subjected  to  com- 
pression. If  the  lung  has  been  compressed  for  a  long  time  or  becomes 
1  Jour,  de  physiol.  el  de  pathol.  gen.,  15,  S.  16-22,  1913. 


532         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

adherent  to  the  chest  wall  in  its  collapsed  condition,  extensive  pulmonary 
fibrosis  is  a  probable  sequence.  Another  factor  which  often  prevents  the 
lung  from  being  restored  to  its  normal  condition  is  fixation  of  the  dia- 
phragm (see  section  on  Diaphragmatis) . 

Symptoms. — Acute  pleurisy  may  be  ushered  in  with  a  chill  or  mere 
chilliness,  followed  by  fever.  In  the  majority  of  the  cases,  however,  the 
first  intimation  of  trouble  is  pain  in  the  side.  The  character  of  the  pain 
is  extremely  variable.  Involvement  of  the  apical  pleura  rarely  causes 
a  sharp  pain  but  as  a  rule  manifests  itself  by  a  sense  of  soreness  or  pain 
in  the  shoulder.  The  latter  is  often  regarded  as  rheumatic.  On  the 
other  hand,  it  may  be  agonizing  in  character  and  every  movement  or 
inspiratory  effort  intensifies  the  stabbing,  lancinating  quality  of  the  pain. 
The  pain  is  usually  referred  to  the  nipple  or  axillary  regions,  but  may  be 
noted  beneath  the  scapula.  If  the  diaphragmatic  area  is  involved  the 
pain  may  be  felt  low  down  in  the  back,  in  the  abdomen,  thus  simu- 
lating acute  appendicitis,  etc.,  or  in  the  neck  (see  p.  43).  The  pain  is, 
as  a  rule,  more  intense  during  inspiration  than  expiration,  but  in  rare 
instances  is  felt  solely  with  the  latter  act.  The  pain  is  nearly  always 
aggravated  by  cough.  The  respirations  are  shallow  and  rapid  in  dry 
pleurisy  if  the  pain  is  severe,  but  breathing  of  this  type  is  to  be  dis- 
tinguished from  true  dyspnea.  The  patient  by  breathing  in  this  rapid 
manner  unconsciously  seeks  to  prevent  the  inflamed  pleural  surfaces  from 
rubbing  together  any  more  than  possible;  it  is  probable  also  that  the 
increased  frequency  of  the  respirations  are  compensatory.  If  cough  is 
present  it  is  usually  short  and  hacking  in  character,  for  the  same  reason 
that  the  respiratory  act  is  hurried,  namely,  the  effort  to  keep  the  in- 
flamed surfaces  apart.  The  cough  is  usually  unattended  by  expectora- 
tion, but  if  the  latter  is  present  it  is  scanty,  and  consists  simply  of 
mucus. 

If  the  pleurisy  is  at  all  severe  it  is  usually  attended  by  fever  up  to 
102  or  103°F.  It  may  be  continuous  from  the  start,  or  slightly  remittent 
in  character  (Fig.  317).  As  the  acute  inflammatory  condition  subsides, 
the  fever  falls  gradually  by  lysis.  In  the  protracted  cases  the  temperature 
tends  to  become  more  markedly  remittent  and  assumes  the  form  of 
hectic  fever. 

The  pulse  rate  is  nearly  always  increased  to  100  and  over  and  irregu- 
larity of  the  pulse  is  not  infrequent. 

The  general  symptoms  are  those  of  an  acute  illness,  namely,  general 
malaise,  mental  dulness  and  headache,  especially  if  the  fever  is  high, 
pallor,  a  distaste  for  food  and  constipation. 

With  the  development  of  an  effusion  the  pain  disappears  entirely  or 
at  most  there  is  a  sensation  of  soreness  which  may  be  elicited  only  by 
pressure  of  the  fingers  over  the  site  of  the  inflamed  area.  If  the 
respirations  are  hurried  in  this  stage  of  the  disease,  they  are  due  to  a  true 
dyspnea  owing  to  compression  of  the  lung.  If,  however,  the  effusion  has 
not  been  preceded  by  pain  and  has  developed  insidiously,  dyspnea  may 
be  absent  or  noticed  only  on  unusual  exertion.  Effusions  of  this  type  often 
fill  the  pleural  sac  without  attracting  attention.  This  is  due  to  the  fact 
that  the  lung  on  the  unaffected  side  has  had  time  to  accommodate  itself 
to  the  increased  work  put  upon  it.  Under  such  circumstances  the  patient 
seeks  relief  because  he  feels  that  he  is  gradually  losing  health,  but  is 
unable  to  localize  his  trouble.     His  symptoms  are  as  a  rule  general,  such 


DISEASES    OF    THE    PLEURA 


533 


as  malaise,  weakness  and  some  perversion  of  the  gastrointestinal  func- 
tions. If  the  effusion  has  persisted  for  some  time,  loss  of  weight  is 
usually  a  prominent  symptom. 

It  has  been  noted  also  that  with  the  development  of  an  effusion  the 
urinary  secretion  is  commonly  reduced  in  amount  and  that  the  urine  is 
concentrated  and  of  a  high  specific  gravity.  With  absorption  of  the 
fluid  the  urine  becomes  increased  in  amount. 

Purulent  effusions  will  be  considered  under  a  separate  heading. 


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Fig.  317. — Acute  tuberculous  pleurisy. 

Physical  Signs. — In  the  great  majority  of  cases  our  attention  is 
directed  to  the  pleura,  because  of  the  location  of  the  pain.  Examination 
will  show  that  the  pleural  inflammation  is  either  the  result  of  some  ob- 
vious pulmonary  affection,  or  that  the  pleurisy  is  either  primary  or  sec- 
ondary to  pulmonary  disease  which  is  masked,  as  for  instance,  tuber- 
culosis. On  the  other  hand,  definite  signs  of  pleural  inflammation  may 
be  present  in  some  cases  without  the  presence  of  pain  or  other  symptoms, 
the  finding  being  purely  accidental.  In  still  other  instances  well-marked 
pain  indicative  of  pleural  inflammation  may  not  be  associated  with  any 
physical  signs  whatsoever. 

Dry  Pleurisy. — Inspection. — If  the  pain  is  at  all  severe  objective 
signs  are  usually  present.  The  breathing  is  shallow  and  hurried.  The 
patient  may  lie  on  the  sound  side,  or  sit  up  and  be  inclined  toward  the 
affected  side  with  the  elbow  pressed  against  the  chest  wall.  Change  of 
posture  intensifies  the  pain.  Examination  of  the  chest  shows  restriction 
of  the  expansion  on  the  affected  side. 


534         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Palpation. — A  friction  fremitus  may  be  felt,  but  this  is  rarely  so. 
If  the  patient  is  examined  from  behind  and  a  hand  is  placed  on  each  side 
of  the  chest  wall,  it  will  be  noted  that  the  inspiratory  excursion  is  much 
diminished  on  the  affected  side.  If  firm  pressure  is  made  with  the  hands, 
some  relief  is  experienced  by  the  patient  as  the  inspiratory  excursion  is 
thus  restricted.  It  is  because  of  this  that  adhesive  strips  are  applied  to 
the  affected  side  in  order  to  diminish  the  pain. 

In  the  comparatively  rare  instances  in  which  inflammation  of  the 
pleura  exists  without  one  being  able  to  hear  a  friction  rub,  its  presence 
may  be  established  by  firm  pressure  with  the  finger  tips  over  the  site 
of  the  pain.  This  procedure  will  often  reveal  distinct  tenderness.  It 
is  also  to  be  noted  that  in  those  cases  in  which  a  friction  rub  is  accident- 
ally discovered  that  some  tenderness  on  pressure  can  usually  be  elicited. 

Percussion. — There  are  no  alterations  in  the  percussion  note  during 
this  stage. 

Auscultation. — The  presence  of  an  audible  friction  rub  is  the  charac- 
teristic feature  of  an  inflamed  pleura.  The  friction  rub  may  be  heard 
over  a  wide  area,  or  it  may  be  localized  in  a  spot  no  larger  than  that  cov- 
ered by  the  bell  of  the  stethoscope. 

The  friction  rub  becomes  audible  as  the  inflamed  surfaces  of  the 
visceral  and  parietal  layers  pass  over  each  other  during  the  respiratory 
act.  In  the  majority  of  cases  it  is  heard  only  during  the  inspiratory 
phase  and  is  usually  most  pronounced  just  as  inspiration  ceases.  It  may 
be  heard,  however,  during  both  inspiration  and  expiration  and  rarely 
the  rub  occurs  during  expiration  only. 

The  friction  rub  suggests  a  rubbing  or  grazing  sound ;  it  may  be  rough 
and  grating  in  character,  or  it  may  resemble  the  sound  produced  by 
creaking  leather. 

The  friction  rub  is  usually  a  very  local  sound  and  is  always  best  heard 
in  those  parts  where  the  respiratory  excursion  is  greatest,  namely,  the 
lower  part  of  the  chest  below  the  nipple,  axilla  or  about  the  angle  of  the 
scapula.  I  have  already  pointed  out  that  the  area  beneath  the  nipple 
and  axilla  is  frequently  the  site  of  pleural  adhesions.  The  most  com- 
mon site  of  pleural  adhesions  is  over  the  apex  posteriorly.  Severe 
pleuritic  pain  is  rarely  experienced  in  this  region,  however,  owing  to 
the  very  limited  movement  of  the  apices  of  the  lungs.  Pain  due  to 
apical  pleurisy  usually  simulates  rheumatic  pain  in  the  shoulder,  or 
muscular  soreness,  and  is  a  common  symptom  of  apical  tuberculosis. 
Soreness  or  tenderness  beneath  the  clavicle  is  a  frequent  occurrence  in 
pulmonary  tuberculosis,  especially  if  cavity  formation  has  taken  place. 

Fibrinous  Pleurisy. — The  physical  signs  during  the  second  stage 
of  £he  inflammatory  process  differ  but  little  from  those  just  described. 
The  only  points  of  difference  lie  in^the  fact  that  dry  pleurisy,  in  which 
the  membrane  is  simply  roughened,  is  chiefly  tuberculous  in  origin  and 
is  not  apt  to  involve  a  large  area  of  the  pleural  surface.  Fibrinous  pleu- 
risy, on  the  other  hand,  while  it  may  be  tuberculous  in  origin  is  seen  in  its 
most  typical  form  when  associated  with  an  acute  inflammatory  condition 
of  the  lung,  particularly  croupous  pneumonia.  When  associated  with 
pneumonia  the  exudate  may  spread  over  the  visceral  layer  of  an  entire 
lobe  of  the  lung.  This  explains  why  one  can  occasionally  detect  some 
impairment  of  resonance  over  a  lung  which  a  day  or  so  later  shows  signs 
of  a  croupous  pneumonia.     Furthermore,  a  widespread  fibrinous  deposit 


DISEASES    OF   THE    PLEURA  535 

will  manifest  itself  by  the  presence  of  a  friction  rub  heard  over  a  wider 
area  than  is  usually  encountered  in  simple  dry  pleurisy.  The  condition 
is  usually  limited  to  one  side  but  it  may  be  bilateral. 

Diaphragmatic  Pleurisy.— This  form  of  pleurisy  is  deserving  of' 
special  mention  because  it  may  simulate  an  acute  abdominal  condition. 
The  diaphragmatic  pleura  may  become  inflamed  as  any  other  portion 
of  the  pleural  surface  or  it  may  be  secondarily  involved  from  the  abdomen. 
The  right  side  is  involved  about  twice  as  often  as  the  left. 

In  inflammation  of  the  diaphragmatic  pleura,  the  subjective  symp- 
toms, as  a  rule,  are  out  of  all  proportion  to  the  objective  signs.  Both 
because  the  lungs  have  the  widest  respiratory  excursion  at  the  base  and 
because  of  the  part  taken  by  the  diaphragm  in  the  respiratory  act,  pleural 
inflammation  in  this  situation  gives  rise  to  the  most  intense  pain  (see 
Fig.  41). 

The  characteristic  feature  of  the  pain  is  that  it  is  referred  to  parts 
distant  from  the  seat  of  the  inflammation.  The  referred  pain  of  dia- 
phragmatic pleurisy  is  due  to  involvement  of  the  spinal  nerves  supplying 
the  abdominal  wall.  The  pain  is,  therefore,  superficial  and  not  deep- 
seated  as  in  visceral  pain.  In  cases  of  diaphragmatic  pleurisy  or  sub- 
phrenic abscess,  steady,  deep  pressure  over  the  gall-bladder  or  appendix 
is  well  borne.  If,  however,  these  organs  are  the  seat  of  inflammatory 
changes  the  deep  pressure  gives  rise  to  severe  pain. 

Capps1  in  a  study  of  61  cases  of  diaphragmatic  pleurisy  found  the 
pain  referred  to  the  gall-bladder  10  times;  lateral  to  and  slightly  above 
the  navel  15  times;  and  other  points,  including  the  lumbar  region,  in  the 
remainder.  If  diaphragmatic  pleurisy  is  suspected,  search  should  be 
made  for  tender  points  in  the  neck  and  shoulder  region  as  referred  pain 
to  these  points  is  commonly  present. 

In  addition  to  the  pain  there  is  usually  some  cough,  expectoration, 
rapid  respirations  and  a  leukocytosis.     Herpes  may  be  present. 

Pleural  Effusion. — Inspection. — Unless  the  fluid  has  accumulated 
rapidly  dyspnea  will  not  be  noted,  otherwise  the  breathing  may  be 
hurried.  Cyanosis  is  rarely  seen  even  when  the  exudation  fills  the  pleural 
sac  in  a  brief  space  of  time.  In  common  with  many  other  inflammatory 
conditions  within  the  thorax  inequality  of  the  pupils  is  not  infrequent, 
the  larger  pupil  being  on  the  same  side  as  the  thoracic  trouble. 

Turning  our  attention  to  the  chest  itself  the  first  thing  to  be  noted  is 
the  respiratory  movements.  If  one  side  is  seen  to  expand  less  than  its 
fellow  the  lack  of  expansion  may  be  due  to  one  of  two  things,  an  acute 
or  chronic  inflammatory  process  (usually  the  latter),  of  the  lung,  or 
fluid  in  the  pleural  sac.  If  the  lung  itself  is  the  cause,  there  is  usually 
some  retraction  of  the  affected  side,  especially  if  the  process  is  chronic 
in  nature.  In  the  case  of  effusion  the  affected  side  appears  larger  and 
the  intercostal  spaces  are  filled  out,  or  even  present  a  bulging  appearance. 
The  difference  in  the  two  sides  of  the  chest  can  be  shown  also  by  means 
of  a  cyrtometer.     Litten's  sign  is  absent  in  pleural  effusions. 

Next  we  have  to  consider  the  position  of  the  apex  beat  of  the  heart. 
It  is  to  be  borne  in  mind  that  displacement  of  the  viscera  constitutes  one 
of  the  most  important  pieces  of  evidence  as  to  whether  a  pleural  effusion 
is  present  or  not.  If  the  apex  beat  is  displaced  to  the  left  it  may  be 
caused  by  one  of  three  things:  (1)  It  may  be  due  to  hypertrophy  or  dila- 
1  Am.  Jour.  Med.  Soc,  March,  1916. 


536         DISEASES    OF    THE   BROXCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

tation  of  the  heart  itself.  It  is  hardly  likely  that  this  would  cause  any 
confusion,  because  of  other  associated  cardiac  signs.  (2)  The  heart  may 
be  pulled  to  the  left  as  the  result  of  a  fibrosis  involving  the  left  lung.  In 
such  a  case,  however,  it  will  be  noted  that  the  left  chest  is  retracted. 
(3)  It  may  be  due  to  a  pleural  effusion  on  the  right  side  which  has  dis- 
placed the  heart  to  the  left.  If  the  heart  is  displaced  to  the  right  it  is 
the  result  of  one  of  two  things:  (1)  A  chronic  fibroid  condition  of  the 
right  lung  which  has  drawn  the  heart  to  the  right;  or  (2)  a  pleural 
effusion  on  the  left  side.  The  apex  beat  may  not  be  visible  either  be- 
cause it  has  been  displaced  to  the  right  and  lies  behind  the  sternum,  or 
because  the  chest  wall  is  so  thick  the  impulse  cannot  be  seen.  Under 
these  circumstances  it  may  be  located  by  palpitation  or  auscultation. 


Fig.  318. — The  first  effect  of  a  small  effusion  is  to  push  the  lung  forward.     Physical  signs 
are  confined  to  the  posterior  aspect  of  chest  and  there  is  no  displacement  of  the  viscera. 

Palpation. — If  there  is  any  doubt  as  to  whether  the  two  lungs  expand 
equally  or  not,  one  can  almost  invariably  arrive  at  a  correct  conclusion 
by  placing  the  hands  on  corresponding  parts  of  the  two  sides  of  the 
chest.  In  this  way  inequalities  of  expansion  can  be  felt  when  they  are 
not  readily  detected  by  the  eye. 

Tactile  fremitus  is  absent  over  the  affected  side  unless  the  underlying 
lung  be  solidified  (see  Fig.  57).  If  the  apex  beat  of  the  heart  is  not 
visible  on  inspection  it  may  be  located  by  palpation. 

Percussion. — In  case  the  effusion  is  small  in  amount  it  is  important 
to  determine  the  lower  limit  of  pulmonary  resonance.  This  is  on  a  level 
with  the  tenth  dorsal  vertebra.  If  it  is  found  to  be  an  inch  or  two  higher 
on  one  side  it  points  to  a  small  effusion  if  there  has  been  a  recent  history 
of  pain  on  that  side.  An  effusion  is  not  apt  to  be  suspected,  however, 
unless  it  has  reached  a  line  corresponding  with  the  angle  of  the  scapula. 

The  percussion  note  over  an  effusion  is  flat  and  being  one  of  the 
varieties  of  dulness  is  high-pitched.  Furthermore,  there  is  a  sensation 
of  resistance  imparted  to  the  finger  acting  as  the  flexor. 


DISEASES    OF    THE    PLEURA 


537 


In  determining  the  extent  of  the  effusion  the  percussion  should  be 
performed  lightly  so  as  to  distinguish  between  the  absolute  dulness  or 
flatness  over  the  fluid  and  the  relative  dulness  over  the  lower  part  of 
the  lung  which  is  collapsed.  The  percussion  should  be  performed  at 
right  angles  to  the  spinal  column  and  at  different  levels,  as  it  has  long  been 
recognized  that  the  fluid  extends  higher  in  one  portion  of  the  chest  than 
in  others.  As  the  fluid  accumulates  in  the  pleural  sac  the  lung  is  pushed 
forward  as  seen  in  Figs.  318  and  319.  In  these  small  effusions  the  dulness 
is  highest  at  the  spine  and  confined  to  the  back,  rarely  extending  anterior 
to  the  posterior  axillary  line.  In  small  effusions  displacement  of  the 
viscera  is  not  apt  to  occur.     It  should  be  borne  in  mind  that  small  effu- 


Fig.  319. — Transverse  section  through  the  nipple  line. 
Diffuse  pulmonary  tuberculosis  in  a  man  aged  25  years,  with  a  bilateral  serofibrinous 
effusion    which    has    accumulated    posteriorly.     The    anterior    pulmonary    margins    show 
vicarious  emphysema  and  completely  overlap  the  heart,  which  is  distended  with  blood 
clots.      (Piroyoff.) 

sions  may  exist  without  their  being  physically  demonstrable.  Experi- 
mentally (post-mortem),  400  c.c.  (§  xiii)  of  fluid  in  the  pleural  cavity  of 
the  adult,  and  120  c.c.  in  a  child  of  twelve  can  be  demonstrated  by  phys- 
ical signs.  Clinically,  even  smaller  amounts  may  be  detected,  but  small 
effusions  may  exist  and  may  be  visible  fluoroscopically  as  a  flattening  of 
the  diaphragm  which  cannot  be  demonstrated  by  physical  signs. 

In  moderate  effusions  the  lowest  level  of  dulness  is  at  the  spine;  it 
then  rises  toward  the  middle  of  the  scapula  and  slopes  downward,  assum- 
ing the  shape  of  the  letter  S  as  it  passes  toward  the  front.  As  the  effusion 
increases  in  size  the  lung  is  floated  and  pushed  upward  and  backward 
toward  the  spine  and  while  the  lower  part  of  the  lung  is  relaxed.  As  a 
result  of  this  the  note  over  the  relaxed  portion  of  the  lung  is  not  dull 
but  has  a  tympanitic  quality,  sometimes  referred  to  as  Skodaic  tympany 


538  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

or  Skoda's  resonance.     The  area  in  which  this  note  is  elicited  is  shown  in 
Fig.  320.     This  space  is  known  as  Garland's  triangle. 

In  massive  effusions  the  highest  point  of  clulness  is  posteriorly  at  the 


Fig.  320. — Showing  area  skodaic  tympany  (Garland's  triangle). 


Fig.  321. — Upper  and  lower  limits  of  dulness  in  a  massive  effusion. 

spine  (see  Fig.  321)  and  lowest  in  the  front  of  the  chest.  Over  the  col- 
lapsed portion  of  the  lung  the  note  may  be  tympanitic  in  character  but 
if  the  lung  has  been  so  completely  compressed  as  to  be  devoid  of  air  the 
note  will  be  dull.     In  massive  effusions  the  flat  or  dull  percussion  note 


DISEASES    OF   THE    PLEURA  539 

anteriorly  may  be  elicited  some  distance  to  the  left  or  right  (as  the  case 
may  be)  of  the  affected  side  (see  Figs.  322  and  323). 

By  the  time  the  effusion  has  reached  any  considerable  amount  dis- 
placement of  the  viscera  will  be  noted.  On  the  right  side  the  weight  of 
the  fluid  flattens  the  diaphragm  and  as  a  result  the  liver  is  forced  clown- 
ward.  This  may  be  noted  by  palpation  or  percussion;  usually  the  latter. 
On  the  left  side  the  filling  of  the  complementary  pleural  space  and  the 
flattening  of  the  diaphragm  sometimes  causes  a  disappearance  of  the 
tympanitic  area  in  the  anterior  and  lower  part  of  the  chest.  This  tym- 
panitic area  is  known  as  Traube's  space  (see  Fig.  89).  Dulness  over  this 
space  is  met  with,  as  a  rule,  in  massive  effusions  only  and  even  then  may  not 
occur  as  the  complementary  pleural  space  is  often  obliterated  by  firm 
adhesions. 


Fig.  322. — Area  of  percussion  dulness  in  a  massive  pleural  effusion.      The  dulness  extends 
beyond  the  middle  line  and  merges  into  cardiac  dulness. 

Movable  dulness,  when  present,  is  a  valuable  sign.  As  a  rule,  it  is 
obtained  in  moderate-sized  effusions  only.  If  the  effusion  extends  in 
front  as  high  as  the  fourth  interspace  when  the  patient. is  sitting  up,  it 
will  be  found  that  when  he  lies  down  the  upper  limit  of  dulness  is  in  the 
interspace  below.  This  is  due  to  the  fluid  gravitating  to  the  most 
dependent  portion  of  the  chest,  namely,  the  back.  Movable  dulness 
cannot  be  demonstrated  in  massive  effusions  extending  to  or  above  the 
second  rib  in  front  nor  in  small  effusions  when  the  sings  are  confounded 
entirely  to  the  back.  Neither  can  it  be  demonstrated  in  moderate- 
sized  effusions  if  the  lung  has  become  adherent.  Movable  dulness  on 
change  of  posture,  when  it  can  be  demonstrated,  is  the  most  pathogno- 
monic physical  sign.  As  a  general  rule,  however,  except  in  cases  oi  hydro- 
pneumothorax,  mobility  of  dulness  is  not  readily  demonstrable  and  con- 


5-AO         DISEASES    OF    THE   BROXCHI,    LUNGS,    PLEURA,    AXD    DIAPHRAGM 

siderable  time  is  often  required  before  the  fluid  gravitates  to  the  lower 
portion  of  the  pleural  cavity. 

A  sign  of  some  value  is  the  paravertebral  triangle  of  dulness,  some- 
times referred  to  as  Grocco's  triangle.  This  triangle  consists  of  an  area 
of  relative  percussion  dulness  on  the  side  opposite  the  effusion.  The 
vertical  line  of  the  triangle  extends  along  the  middle  of  the  spinal  column 
from  a  point  slightly  above  the  upper  level  of  the  effusion  to  the  tenth 
dorsal  vertebra,  the  latter  representing  the  lower  limit  of  pulmonary  res- 
onance; the  base  of  the  triangle  extends  outward  along  the  lower  limit 


Fig.  323. — Left-sided  hydrothorax  and  hydropericardium.  1,  Esophagus.  2,  Aorta. 
3,  Inferior  vena  cava.     4,  Liver.     5,  Heart. 

The  cardiac  apex  is  displaced  backward  and  to  the  right.  The  left  pleural  sac  extends 
anteriorly  to  the  mid-sternal  line,  and  posteriorly  even  beyond  it.      (After  Pirogoff.) 

of  normal  pulmonary  resonance  for  a  distance  varying  from  1  to  3  inches; 
the  hypothenuse  joins  these  two  lines  (see  Fig.  324).  The  dulness  is 
more  marked  over  the  spine.  There  is  some  doubt  as  to  how  this 
triangular  area  of  dulness  is  produced.  The  generally  accepted  view, 
however,  is  that  the  contents  of  the  posterior  mediastinum  are  displaced 
(see  Fig.  323).  The  chief  value  of  this  sign  is  in  differentiating  between 
pleural  effusions  and  tumors  involving  the  lung  or  pleura;  if  present,  it 
is  not  likely  that  a  tumor  exists. 

Auscultation. — The  characteristic  friction  rub  heard  at  the  base  of 
the  chest  in  the  dry  and  fibrinous  stage  disappears  as  the  two  pleural 
surfaces  are  separated  by  the  effusion.  A  friction  rub  may  be  heard, 
however,  just  above  the  fluid  in  the  axilla  or  anterior  and  superior  por- 
tion of  the  chest  where  the  inflamed  pleural  surfaces  are  still  in  contact. 
Over  the  area  occupied  by  the  effusion  the  breath  sounds  may  be  weakly 
vesicular  or  bronchial  in  character.  As  the  fluid  increases  in  amount 
the  breath  sounds  tend  to  become  more  and  more  distant  and  in  massive 


DISEASES    OF    THE    PLEURA 


541 


effusions  may  be  entirely  absent.  In  a  certain  proportion  of  cases, 
especially  when  the  effusion  is  large,  loud  bronchial  breathing  may  be 
heard.     For  the  explanation  of  this  phenomenon  see  page  60. 

In  addition  to  the  friction  rub  heard  above  the  level  of  the  effusion, 
rales  produced  within  the  lung  may  be  heard  in  the  same  areas.  The 
pulmonary  rales  may  be  due  to  congestion  in  the  collapsed  portion  of 
the  lung  or  they  may  be  due  to  the  separation  of  the  walls  of  the  finer 
bronchioles  and  alveoli  in  the  atelectatic  portion  of  the  lung.  The 
breath  sounds  above  the  effusion  are  usually  of  a  harsh  broncho-vesicular 
character. 


Slight   tympany  with 
exaggerated  breath 
sounds 


Dulness,  distant  bron- 
chial breathing  and 
egophony 


Flatness,  with  absent 
vocal  resonance  and 
fremitus,  as  well 
as  breath  sounds 


Fig.  324. 


On  auscultation  of  the  voice  sounds,  the  same  phenomena  are  en- 
countered as  in  auscultation  of  the  breath  sounds.  The  spoken  voice 
may  have  a  distant  sound  or  it  may  be  distinctly  bronchophonic.  Just 
as  in  the  case  of  the  breath  sounds  a  very  large  accumulation  of  fluid 
may  cause  complete  disappearance  of  the  voice  sounds.  The  presence 
of  egophony,  while  not  a  constant  finding,  occurs  with  great  frequency 
in  association  with  pleural  effusion. 

In  some  instances  auscultation  of  the  whispered  voice  is  of  service 
in  distinguishing  between  serous  and  purulent  effusions.  If  the  effusion 
is  serous,  one  will  be  able  to  hear,  at  times,  the  whispered  voice  trans- 
mitted through  the  fluid  but  if  the  effusion  is  purulent  no  such  transmis- 
sion occurs.  This  sign,  known  as  Baccelli's,  is,  however,  of  relatively 
little  value. 

In  not  a  few  instances  the  question  of  whether  the  heart  is  displaced 


542         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

or  not  will  depend  on  the  use  of  the  stethoscope.  In  spite  of  the  great 
displacement  of  the  heart  which  sometimes  occurs,  the  cardiac  sounds  are 
usually  normal. 

Exploratory  Puncture. — -No  matter  how  positive  the  evidence  is  as 
to  the  presence  of  fluid  in  the  pleural  cavity  the  use  of  an  exploratory 
needle  should  never  be  omitted.  There  are  two  reasons  for  this.  In 
the  first  place  the  actual  demonstration  of  fluid  by  means  of  the  needle 
clinches  the  diagnosis.  In  the  second  place  our  duty  to  the  patient  does 
not  end  with  the  discovery  of  the  presence  of  fluid  nor  is  our  work  com- 
pleted until  the  character  of  fluid  has  been  demonstrated.  Inasmuch  as 
we  can  never  tell,  with  any  degree  of  certainty,  whether  the  fluid  is 
serous  or  purulent,  the  needle  must  be  resorted  to.  If  purulent  fluid  is 
withdrawn,  immediate  drainage  of  the  pleural  cavity  is  mandatory,  if 
the  patient  is  to  escape  the  horrors  of  a  chronic  empyema. 

In  making  an  exploratory  puncture  of  the  pleura  or  lung  the  areas 
in  which  the  viscera  are  located  should  be  kept  in  mind.  In  the  great 
majority  of  instances  when  fluid  is  suspected  the  exploring  needle  is 
inserted  in  an  interspace  just  below  or  slightly  anteriorly  to  the  angle  of 
the  scapula.  If  too  fine  a  needle  is  used  a  dry  tap  may  result  if  the  fluid 
consists  of  thick  pus.  For  this  reason  the  needle  should  have  a  caliber 
of  at  least  2  mm. 

Sterilization  of  the  skin  with  tincture  of  iodine  and  the  use  of  a  sterile 
needle  renders  the  procedure  entirely  harmless.  Even  if  fluid  is  not 
present  and  the  needle  punctures  the  lung,  no  harm  will  result  providing 
the  rules  for  cleanliness  have  been  observed. 

The  X-rays  are  helpful  as  a  diagnostic  measure,  especially  in  case  the 
effusion  is  loculated. 

Physical  Signs  Following  Absorption  of  the  Exudate.- — Even  in  those 
cases  in  which  the  effusion  exists  but  a  relatively  short  time  the  lung 
does  not  expand  immediately  to  its  former  state  following  removal  of 
the  fluid.  If  the  effusion  has  existed  for  several  weeks  before  it  is  dis- 
covered and  removed,  or  if  it  is  allowed  purposely  to  remain  and  undergo 
spontaneous  absorption,  it  may  take  several  months  for  the  lung  to  be- 
come completely  reexpanded.  If,  therefore,  the  case  is  seen  after  ab- 
sorption of  the  fluid  and  before  the  lung  has  reexpanded  confusion  may 
arise  unless  the  morbid  anatomy  and  the  physical  signs  associated  with 
this  phase  of  the  process  are  kept  in  mind  (see  p.  595). 

If  the  effusion  has  followed  an  attack  of  dry  pleurisy  the  lung  will 
usually  reexpand  without  the  formation  of  pleuritic  adhesions  or  at  the 
most  the  adhesions  will  be  slight. 

If  a  fibrinous  exudate  has  been  the  starting  point  of  the  effusion  and 
especially  if  the  fibrinous  deposit  has  been  extensive  the  two  pleural 
surfaces  may  become  firmly  adherent  following  absorption  of  the  fluid 
and  then  prevent  complete  reexpansion.  Chronic  obliterative  pleurisy 
probably  originates  in  this  way  in  the  majority  of  cases. 

Following  spontaneous  absorption  of  the  pleural  exudate  or  its  re- 
moval by  paracentesis  the  following  physical  signs  will  be  noted : 

Inspection. — Expansion  on  the  affected  side  will  be  restricted  but  if 
the  patient  has  been  seen  from  the  onset  the  respiratory  excursion  will 
be  greater  than  when  the  effusion  was  present.  Flattening  and  bulging 
of  the  interspace  will  have  disappeared  and  the  apex  beat  of  the  heart 
will  be  seen  in  its  normal  position. 


DISEASES    OF    THE    PLEURA  543 

Palpation. — Tactile  fremitus  may  or  may  not  be  present,  depending 
on  how  much  the  lung  has  expanded. 

Percussion. — rThe  percussion  note  will  still  be  dull  over  the  base  of 
the  lung  posteriorly.  It  will  be  found,  however,  that  the  dull  area  does 
not  conform  to  the  shape  noted  when  fluid  was  present.  As  the  dia- 
phragm is  relieved  of  the  weight  of  the  fluid,  the  liver  is  no  longer  de- 
pressed and  the  tympanitic  note  over  Traube's  space  returns.  Tympany 
may  replace  dulness  elsewhere. 

Auscultation. — At  the  base  of  the  affected  side  the  breath  sounds  are 
still  absent  or  distant  but  not  over  such  a  wide  area,  and  the  same  is 
true  of  the  voice  sounds.  With  the  removal  of  the  fluid  a  friction  rub 
again  becomes  audible  especially  in  the  area  about  the  angle  of  the  scapula. 
Deep  breathing  may  bring  out  fine  crepitant  rales  as  the  result  of  forcible 
distention  of  the  atelectatic  portion  of  the  lung. 

This  picture  may  remain  unchanged  for  weeks  or  months.  Gradu- 
ally, however,  unless  the  lung  has  been  bound  down  by  adhesions,  the 
complementary  pleural  space  obliterated  or  the  diaphragm  rendered 
immobile,  these  signs  disappear  and  leave  little  or  no  evidence  of  damage. 
It  is  desirable  to  examine  such  cases  with  the  fluoroscope  as  the  persistence 
of  the  abnormal  physical  signs  may  be  due  to  changes  in  the  diaphragm. 

Diagnosis. — In  the  dry  and  fibrinous  stages  pleurisy  may  be  confused 
with  intercostal  neuralgia,  pleurodynia  and  herpes  zoster. 

In  intercostal  neuralgia  there  is  absence  of  fever  and  a  friction  rub. 
The  pain  while  localized  is  darting  and  neuralgic  in  character  and  tender- 
ness is  present  at  the  points  of  exit  of  the  intercostal  nerves.  Occasion- 
ally these  phenomena  precede  an  attack  of  herpes  zoster. 

In  pleurodynia  the  pain  is  confined  to  one  side  but  is  not  so  sharply 
localized  as  pleurisy  and  it  may  leave  one  side  and  affect  the  other. 
Muscular  movement  as  well  as  breathing  aggravates  the  pain.  Tender- 
ness on  pressure  is  usually  present.  There  is  neither  fever  nor  a  fric- 
tion rub. 

When  the  pleural  effusion  develops  rapidly  and  the  attack  is  abrupt 
in  onset  with  pain  in  the  side,  fever,  hurried  respirations,  and  bronchial 
breathing  over  one  lung,  it  must  be  distinguished  from  croupous  pneu- 
monia. It  is  remarkable  how  many  cases  of  acute  pleurisy  with  effusion 
escape  notice.  A  very  large  proportion  of  cases  of  croupous  pneumo- 
nia with  delayed  resolution  are  probably  of  this  nature.  The  acuteness 
of  the  attack  and  the  bronchial  breathing  can  very  easily  cause  the  un- 
wary to  make  a  mistake.  Later  as  the  effusion  absorbs  and  abnormal 
physical  signs  persist  in  the  base  of  the  lung  it  is  assumed  that  resolution 
of  the  pneumonia  has  been  delayed.  In  this  connection  it  might  be 
stated  that  as  a  sequel  of  pneumonia,  delayed  resolution  is  a  very  rare 
occurrence. 

In  doubtful  cases  the  differentiation  between  pleurisy  with  effu- 
sion and  croupous  pneumonia  rests  upon  two  facts.  (1)  Displacement  of 
the  viscera,  and  (2)  the  use  of  an  exploring  needle.  In  pleurisy  the  vis- 
cera are  displaced  while  in  croupous  pneumonia  they  are  not.  If  an  effu- 
sion is  present  serous  or  purulent  fluid  is  obtained  with  the  exploring 
needle  while  if  pneumonia  is  present  a  few  drops  of  dark  red  blood  maj' 
appear  in  the  syringe. 

Malignant  disease  of  the  lung  or  pleura  is  relatively  uncommon  but 
when  it  involves  a  lower  lobe  is  more  frequently  mistaken  for  a  pleural 


544         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

effusion  than  any  other  condition.  This  is  due  to  the  fact  that  the  tumor 
mass  gives  an  absolutely  fiat  note  devoid  of  any  semblance  of  resonance 
and  both  the  voice  and  breath  sounds  are  very  distant  or  absent.  In 
such  a  case  one's  suspicion  might  be  aroused  by  the  absence  of  the  para- 
vertebral area  of  dulness  on  the  opposite  side.  As  this  sign  is  sometimes 
absent  in  the  presence  of  an  effusion  it  cannot  be  relied  on  absolutely. 

Here  again  the  displacement  of  the  viscera  and  the  exploring  needle 
are  our  main  reliance  in  escaping  an  error  in  diagnosis. 

Chronic  Pleurisy. — Two  forms  of  chronic  pleuritis  are  recognized: 
(1)  Persistent  reaccumulation  of  serofibrinous  or  purulent  fluid  after  re- 
peated tappings  or  operation  Reaccumulation  of  a  serofibrinous  effusion 
is  not  uncommon  in  tuberculosis  and  malignant  disease.  In  addition  an 
effusion  which  has  been  allowed  to  remain  in  the  chest  too  long  shows  a 
marked  tendency  to  reaccumulate.  In  a  case  which  came  under  my  care 
a  massive  effusion  had  gone  unrecognized  for  four  months.  Although 
tapped  frequently  the  fluid  rapidly  reaccumulated  after  each  operation. 

(2)  Chronic  dry  pleurisy  is  a  common  sequel  of  the  acute  fibrinous 
type  and  effusions  either  serofibrinous  or  purulent.  It  is  also  very  fre- 
quently seen  in  association  with  chronic  pulmonary  tuberculosis.  Partial 
obliteration  of  the  pleural  sac  is  seen  most  often  at  the  apices  of  the  lung 
and  is  almost  constantly  present  in  tuberculosis.  Over  the  lower  lobes 
an  obliterating  pleurisy  is  also  common  but  the  adhesions  are  less  dense. 
In  the  majority  of  such  instances  the  adhesions  are  delicate,  lace-like 
and  easily  broken  up.  Among  197  autopsies  at  the  Phipps  Institute 
obliterating  pleuritis  was  noted  49  times  over  the  left  lower  lobe  and  71 
times  over  the  right  lower  lobe.  Dense  thickening  of  the  pleura  over  the 
lower  lobes  is  usually  associated  with  massive  fibrosis  of  the  lung  and  is 
often  a  sequel  of  an  effusion,  especially  the  purulent  type.  Chronic 
pleurisy  usually  has  reference  to  that  portion  of  the  pleura  which  over- 
lies the  lower  lobes  of  the  lungs. 

Chronic  thickening  of  the  pleura  is  a  diagnosis  which  is  frequently 
made  to  explain  restriction  of  motion,  impairment  of  the  percussion  note 
and  more  or  less  suppressed  breath  sounds  at  the  base  of  the  lung  poste- 
riorly. Personally,  I  have  rarely  seen  at  the  autopsy  table  thickening 
of  the  pleura  sufficient  to  account  for  these  signs.  Even  in  those  cases 
in  which  there  has  been  any  marked  degree  of  thickening  the  lung  was 
also  involved  in  the  chronic  inflammatory  process.  Probably  the  most 
important  factor  in  giving  rise  to  these  physical  signs,  especially  after 
effusions,  is  immobility  of  the  diaphragm.  The  diaphragm  may  have 
been  implicated  in  the  inflammatory  process  or,  what  is  not  uncommon, 
adhesions  may  have  formed  between  the  chest  wall  and  the  diaphragm 
thus  obliterating  the  phreno-costal  sulcus.  As  a  result  the  movement  of 
the  diaphragm  is  interfered  with.  The  effect  of  inflammatory  conditions 
on  the  diaphragm  has  been  considered  in  detail  in  the  section  on  "  Diseases 
of  the  Diaphragm." 

EMPYEMA 

(Purulent  pleurisy,  pyothorax) 

This  is  one  of  the  varieties  of  pleuritis ;  but  in  view  of  certain  patholog- 
ical peculiarities  it  seems  best  to  consider  it  as  a  distinct  disease. 
Furthermore,  it  is  usually  secondary  to  conditions  in  which  from  the  very 
onset,  there  is  a  decided  tendency  toward  the  formation  of  pus. 


DISEASES    OF    THE    PLEURA 


545 


Etiology. — The  organism  which  most  frequently  causes  the  condition 
is  the  pneumococcus.  In  children  the  percentage  is  very  high.  Strep- 
tococci rank  next  in  importance.  A  number  of  studies  that  have  been 
made  of  the  bacteriology  of  empyemata  show  that  from  one-half  to  two- 
thirds  of  the  cases  are  due  to  the  pneumococcus  and  about  one-quarter 
to  the  streptococcus. 

Whether  the  tubercle  bacillus  alone  can  cause  an  empyema  is  not  clear. 
In  a  certain  proportion  of  cases  tubercle  bacilli  can  be  demonstrated  in 
the  fluid  but  usually  in  association  with  other  organisms.  The  so-called 
sterile  purulent  effusions  are  nearly  always  associated  with  a  tuberculous 
process.  Occasionally  the  influenza  bacillus  is  found  in  pure  culture  and 
more  rarelv  other  bacteria. 


Fig.  325. — Empyema — shows  the  right  lung  which  has  become  completely  atelectatic 
{Courtesy  of  Dr.  W.  J.  Calvert.) 

As  an  exciting  cause  of  empyema,  croupous  pneumonia  easily  ranks 
first.  Empyema  is  also  a  relatively  common  complication  of  tuberculosis. 
In  certain  of  the  infectious  diseases,  notably  scarlet  fever,  the  condition 
is  not  infrequently  met  with.  Empyema  may  arise  also  as  the  result  of 
penetrating  wounds  of  the  chest  wall  or  as  the  result  of  disease  involving 
the  mediastinum. 

Morbid  Anatomy. — In  pneumococcic  empyemata  the  effusion  consists 
of  a  thick  creamy  pus  having  a  sweetish  odor.  When  allowed  to  stand 
the  fluid  separates  into  a  clear,  greenish  yellow,  upper  layer,  the  cellular 

35 


546         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

elements  sinking  to  the  bottom.     When  due  to  the  streptococcus  the 
fluid  may  be  only  turbid  in  appearance. 

An  empyema  is  most  apt  to  develop  as  the  result  of  an  extensive 
fibrinous  exudate  such  as  occurs  in  pneumonia  where  the  membrane  is 
thick  and  presents  a  shaggy  appearance.  In  tuberculous  cases  the 
effusion  may  be  changed  from  a  serous  to  a  purulent  one  as  the  result  of 
infection  from  the  lung.  The  effusion  may  be  massive,  filling  the 
entire  pleural  sac  (see  Figs.  325  and  326),  or  it  may  occupy  but  a  portion 
thereof.     Encapsulated  effusions  are  considered  separately. 


Fig.  326. — Massive  left-sided  empyema  occupying  practically  the  whole_  pleural 
cavity.  The  lung  is  represented  by  two  small  fibrous  masses  adherent  to  the  pericardium 
which  contains  a  small  serous  effusion.  The  heart,  which  is  enlarged,  is  filled  with  blood 
clot.  The  diaphragm  is  pushed  downward  and  the  right  lung  greatly  compressed. 
(Pirogoff.) 

Unless  the  purulent  material  is  removed  within  a  short  time  from  its 
onset  the  lower  portion  of  the  lung  in  contact  with  the  fluid  becomes 
firmly  adherent  to  the  chest  wall  and  mediastinum.  The  adhesions  be- 
come organized  very  quickly  and  the  lung  is  thus  firmly  anchored  and 
prevented  from  reexpanding  even  when  the  fluid  is  removed.  The  longer 
the  purulent  material  is  allowed  to  remain  the  more  certain  it  becomes 
that  the  lung  cannot  be  reexpanded.  If  the  empyema  has  existed  for 
several  months  the  parietal  pleura  forming  the  sac  becomes  greatly  thick- 
ened and  in  places  may  become  eroded.  In  moderate-sized  effusions  after 
the  lung  has  become  adherent  the  fluid  is  then  completely  walled  off  and 
really  constitutes  an  abscess  (see  Figs.  327  and  328).     The  effusion  may 


DISEASES    OF    THE    PLEURA 


547 


remain  indefinitely  the  patient  eventually  succumbing  as  the  result  of 
septic  absorption.  In  not  a  few  cases  the  purulent  material  is  gradually 
absorbed.  Following  absorption  of  the  pus  calcium  salts  in  the  form  of 
plates  are  frequently  deposited  at  the  base  of  the  cavity.  In  rarer  in- 
stances the  pus  ruptures  into  the  lung  and  is  discharged  externally  through 


Fig.  321 


-Empyema  encysted  in  lower  part  of  chest.      Note  the  flattening  and  low  posi- 
tion of  the  diaphragm  and  the  downward  displacement  of  the  liver. 


a  bronchus  or  it  may  rupture  externally  through  the  chest  wall — em- 
pyema necessitatis  (see  Fig.  329) . 

Infection  of  both  pleural  sacs  simultaneously  is  very  rare.  I  have 
met  with  one  such  instance  in  which  a  bilateral  croupous  pneumonia  was 
followed  by  a  bilateral  purulent  effusion. 

In  considering  the  morbid  anatomy  of  pleurisy  it  was  pointed  out  that 


548  DISEASES    OF    THE    BROXCHI,    LEXGS.    PLEURA.    AND    DIAPHRAGM 


.&■*£? 


Fig.  328. — Pyothorax  (right-sided).  1,  Esophagus.  2,  Descending  aorta.  3,  Right 
auricle.     4,  Right  ventricle.      5,  Left  auricle.      6,  Left  ventricle. 

The'heart  is  displaced  to  the  left  and  rotated  on  its  long  axis.  The  left  lung  is  pushed 
backward  and  no  longer  overlaps  the  heart.     The  esophagus  is  also  displaced  to  the  left. 


Fig.  329. — Empyema  necessitatis. 


DISEASES    OF    THE    PLEURA  549 

the  lung,  as  the  result  of  pressure,  became  partially  or  completely  col- 
lapsed. If  the  pressure  is  maintained  for  too  long  a  period,  the  atelec- 
tatic part  undergoes  fibroid  changes.  Prolonged  compression  of  the  lung 
by  a  purulent  effusion  is  probably  one  of  the  commonest  causes  of  uni- 
lateral fibrosis  of  the  lung. 

Pryor1  has  recently  called  attention  to  a  phase  of  empyema  to  which 
little  notice  has  been  paid,  namely,  the  crippling  effect  the  disease  often 
has  on  the  diaphragm.  When  empyema  develops  diaphragmatis  is  apt  to 
ensue.  The  diaphragm  becomes  swollen,  thickened  and  stiff.  As  the 
result  of  inflammatory  changes  it  loses  its  elasticity  and  becomes  rigid ; 
later  it  becomes  atrophied,  the  tissues  undergoing  fibroid  changes  and 
becoming  hardened  (see  p.  592).  If  the  effusion  is  large  the  weight  of  the 
fluid  may  flatten  the  diaphragm  or  cause  it  to  become  concave  in  shape. 

Symptoms. — The  onset  of  a  purulent  effusion  may  be  abrupt  as  in  the 
case  of  serous  fluid.  When  empyema  occurs  as  a  complication  of  one  of 
the  acute  infections,  notably  pneumonia,  the  exudation  of  the  purulent 
fluid  may  be  very  rapid,  and  a  very  considerable  amount  may  accumulate 
as  early  as  the  fourth  or  fifth  day  of  the  disease.  Not  frequently,  how- 
ever, it  has  an  insidious  onset  and  is  unsuspected,  either  because  it  devel- 
ops during  the  course  of  other  diseases  or  supervenes  upon  a  preexisting 
serous  effusion. 

In  the  acute  cases  the  symptoms  are  practically  identical  with  acute 
pleurisy.  If  the  onset  of  the  empyema  is  gradual,  respiratory  symptoms 
may  be  wanting  entirely.  Cough  may  or  may  not  be  present  and  unless 
the  effusion  is  very  large  there  will  be  no  dyspnea.  Some  loss  of  weight, 
malaise  and  anemia  are  usually  present.  Sweating  and  irregular  fever 
are  common,  especially  in  children. 

In  the  great  majority  of  cases  of  empyema  there  is  a  well-marked 
polynuclear  leukocytosis.  This  fact  will  often  serve  to  distinguish  be- 
tween serous  and  purulent  effusions,  although  it  is  to  be  borne  in  mind 
that  there  may  be  a  low  white  count  even  in  the  presence  of  pus. 

Physical  Signs. — For  the  most  part  the  physical  signs  which  occur  in 
cases  of  empyema  are  identical  with  those  encountered  in  cases  of  serous 
effusion.  There  are  in  addition,  however,  several  additional  features 
which  are  worthy  of  note. 

Inspection. — Except  in  the  acute  cases,  an  individual  suffering  from  an 
empyema  is  apt  to  reveal  the  evidences  of  a  chronic  suppurative  process, 
namely,  fever,  sweating,  loss  of  vigor,  always  some  emaciation,  and  anemia. 
In  chronic  empyema  clubbing  of  the  fingers  is  often  a  marked  feature  of 
the  disease  and,  in  common  with  bronchiectasis  and  congenital  heart 
disease,  furnishes  the  most  extreme  grades  of  the  condition  encountered. 
In  cases  of  empyema  the  clubbing  of  the  fingers  may  develop  very  rap- 
idly and  instances  have  been  recorded  in  which  the  condition  was  apparent 
within  two  or  three  weeks.  It  has  been  noted  also  that  the  clubbing  dis- 
appears with  the  removal  of  the  pus  from  the  pleural  cavity. 

Bulging  of  the  affected  side  and  of  the  interspaces  is  more  frequently 
encountered  in  cases  of  purulent  than  in  the  case  of  serous  effusions,  due, 
in  all  probability,  to  the  greater  weight  of  the  fluid.  In  children  bulging 
of  the  affected  side  may  be  very  distinct.  Tenderness  on  pressure  is 
commonly  present.  For  some  reason  displacement  of  the  heart  is  apt  to 
be  more  marked.  If  the  empyema  has  existed  for  some  time,  the  small 
1  International  Clinics,  June,  1916. 


550  DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

subcutaneous  veins  on  the  affected  side  may  be  very  noticeable.  Edema 
of  the  chest  wall  is  frequently  met  with.  In  a  certain  proportion  of 
cases  of  pulsation  of  the  chest  wall  is  noted  over  the  area  overlying  the 
empyema  (see  Figs.  105  and  107). 

Pulsating  empyemata,  while  not  invariably  so,  are  in  the  vast  majority 
of  cases  left-sided.  Levi1  found  that  the  left  side  was  the  seat  of  a  pulsat- 
ing effusion  in  93.6  per  cent,  of  110  cases.  In  a  few  instances  pulsation  is 
seen  in  cases  of  serous  effusion.  The  condition  occurs  more  frequently 
in  men  than  in  women.  In  about  one-half  of  the  cases  the  effusion  occurs 
as  a  complication  of  pulmonary  tuberculosis;  next  to  tuberculosis  pneu- 
monia is  the  most  frequent  exciting  cause.  Although  the  pulsation  is 
synchronous  with  the  cardiac  systole  no  satisfactory  explanation  has  been 
forthcoming  as  to  how  the  heart  impulse  is  transmitted  through  the 
effusion. 


<§£) 


('*!*) 


Fig.   330. — Encapsulated  empyema   (necessitatis)    discharging  into   subcutaneous   tissues 
between  seventh  and  eighth  ribs.      (Ashhurst,  International  Clinics,  vol.  iv,  26th  Series.) 

Less  frequently  a  localized  tumor  is  seen  on  the  chest  wall  caused  by 
the  burrowing  of  the  pus  through  the  thoracic  parietes  (Figs.  329  and 
330).  This  is  known  as  empyema  necessitatis.  Complete  perforation  of 
the  chest  wall  may  result  in  the  formation  of  a  fistula.  An  empyema 
necessitatis  is  often  pulsating  in  character.  Of  95  cases  of  pulsating 
empyema  analyzed  by  Sailer2  there  was  in  addition,  an  empyema  neces- 
sitatis in  38.  When  an  empyema  necessitatis  develops  it  almost  invari- 
ably appears  on  the  anterior  or  lateral  chest  wall,  somewhere  between 
the  third  and  sixth  interspaces. 

Palpation. — The  presence  of  edema  may  be  demonstrated  by  pres- 
sure with  the  finger  tips  when  it  would  not  otherwise  be  suspected. 

Percussion. — -In  cases  of  empyema  the  liver  dulness  usually  extends 
much  farther  below  the  margin  of  the  ribs  than  in  cases  of  serous  effusion. 

1  Centralblatt  f.  d.  Grenzgebiete  d.  med.  u.  (Mr.,  xviii,  Xo.  3,  1914. 

2  Am.  Jour.  Med.  Sc,  cxxviii,  225,  1904. 


DISEASES    OF    THE    PLEURA 


551 


This  is  due  to  the  greater  weight  of  the  fluid  which  not  only  flattens  the 
convexity  of  the  upper  surface  of  the  diaphragm  but  may  even  cause  it  to 
become  concave. 

Auscultation. — The  same  variations  in  the  character  of  the  breath 
sounds  occur  in  empyema  as  in  serous  effusions.  The  respiratory  mur- 
mur may  be  faintly  heard  or  entirely  absent.  Occasionally,  and  espe- 
cially in  children  with  a  large  effusion,  the  breathing  may  be  loud  and 
bronchial  in  character. 

The  transmission  of  the  whispered  voice  through  a  serous  effusion  and 
the  absence  of  such  transmission  in  case  pus  is  present,  Baccelli's  sign, 
has  been  alluded  to.     The  sign  is  of  no  great  value. 

Diagnosis. — In  a  patient  with  the  physical  signs  of  a  pleural  effusion 
and  in  whom  there  are  symptoms  of  sepsis,  it  is  highly  probable  that  an 
empyema  is  present.  The  use  of  an  exploring  needle  will  definitely 
decide  the  matter. 

LOCULATED  OR  ENCAPSULATED  EMPYEMA 

An  encapsulated  collection  of  fluid,  almost  always  purulent,  but  some- 
times serous  in  character,  may  occur  in  one  of  the  fissures  between  the 


Fig.  331. — Encysted  empyema  between  upper  and  middle  lobes.  At  operation  the 
abscess  wall  was  tough  and  almost  cartilaginous.  About  2  ounces  of  creamy,  fetid  pus 
was  removed.     (Dr.  D.  R:  Bowen.) 

lobes  of  the  lung,  between  the  diaphragm  and  under  surface  of  the  base 
of  the  lung,  between  the  lung  and  pericardium,  or  as  the  result  of  ad- 


552  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEF/RA,    AND    DIAPHRAGM 

hesions  forming  pockets  between  the  visceral  and  parietal  layers  of  the 
pleura.  The  latter  may  occur  at  any  point  within  the  pleural  sac  but 
are  found  most  commonlv  in  the  lower  and  posterior  aspects  of  the  chest 
(see  Figs.  331,  332,  333,  334). 

Inasmuch  as  a  collection  of  pus  in  one  of  the  interlobular  fissures  is 
not  uncommon,  it  is  important  to  keep  in  mind  the  position  of  these 
fissures.  Figs.  335  and  336  show  their  location.  Fig.  336  shows  the 
complementary  pleural  space  posteriorly. 


Fig.  332. — Localized  apical  empyema.      (Dr.  D.  R.  Bowen.) 

Etiology. — Fluid  may  become  encysted  in  any  one  of  the  sites  above 
mentioned  under  the  same  conditions  under  which  free  pus  in  the  pleural 
sac  or  a  pulmonary  abscess  occurs.  The  condition  is  considered  as  being 
relatively  rare.  Among  35,900  admissions  to  the  City  Hospital,  of  St. 
Louis,  Elsworth  Smith1  reports  87  cases  of  empyema  and  of  this  number 
3  or  3.4  per  cent.,  were  of  the  encysted  type.  Lord2  found  practically 
the  same  percentage,  3.2,  in  248  cases  of  empyema.  On  the  other  hand, 
James3  of  Edinburgh,  has  reported  19  instances  of  encapsulated  fluid 
among  43  cases  of  empyema.  By  most  observers  the  term  encapsulated 
empyema  is  restricted  to  small  collections  of  pus  located  in  the  inter- 
lobar fissures  or  between  the  lung  and   the  diaphragm  while  relatively 

1  Jour.  Am.  Med.  Assoc,  Dec.  7,  1912. 

2  "Diseases  of  the  Bronchi,  Lungs  and  Pleura,"  p.  531,  1915. 

3  "Pleurisy,"  p.  139. 


DISEASES    OF    THE    PLEURA 


553 


Fig.  333. — Empyema  encapsulated  at 
base  of  left  lung.  Sagittal  section  of  thorax 
through  middle  of  left  clavicle.  {Ashhurst, 
International  Clinics,  vol.  iv,  26th  Series.) 


Fig.  334. — Diagram  of  sagittal  section 
through  middle  of  left  clavicle,  indicating 
site  at  which  pus  was  found  at  autopsy. 
(Ashhurst,  International  Clinics,  vol.  iv, 
26th  Series.) 


Fig.   335. — Anterior  view  of  fissures  of  lungs.  Fig.  336. — Posterior  view  of  fissures  of 

Dotted  lines  indicate  the  pleura.  lungs.      Dotted  lines    indicate    lower   limit 

of  pleural  sacs. 


554         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

large  purulent  effusions  which  may  occupy  as  much  as  half  the  pleural 
cavity  are  classed  as  ordinary  empyemas.  Ashhurst1  very  properly 
points  out  that  with  the  .exception  of  massive  empyemas,  the  pus  is  al- 
ways encapsulated  (see  Figs.  327  and  328).  Adhesions  are  quickly 
formed  between  the  lung  and  adjacent  structures  and  in  this  way  the 
pus  is  walled  off.  In  some  instances  the  resulting  vomica  is  small,  in 
others  it  may  occupy  a  large  portion  of  the  pleural  cavity.  In  rare  in- 
stances the  encysted  fluid  is  serofibrinous  in  character.  Pleural  effusions 
which  arise  as  the  result  of  a  transudate  (heart  and  renal  disease)  never 
become  encapsulated. 


($D 


(jg) 


Fig.  337. — Interlobar  empyema  ruptured  into  a  bronchus  (pleural  vomica).  Note 
pleural  effusion  in  costo-phrenic  sinus.  (Ashhurst,  International  Clinics,  vol.  iv,  26th 
Series.) 


Morbid  Anatomy. — As  the  result  of  a  fibrinous  exudate  adhesions 
may  take  place  at  the  circumference  of  the  inflammatory  area  thus  wall- 
ing off  the  fluid  if  any  arises.  This  may  occur  between  the  under  surface 
of  the  lung  and  the  diaphragm  or  at  any  point  over  the  antero-  or  postero- 
lateral aspects  of  the  lung.  In  like  manner  the  exudate  may  extend 
slightly  into  one  of  the  fissures  dividing  the  lobes.  In  the  latter  instance 
if  adhesions  occur  a  closed  pocket  is  produced. 

In  many  instances  what  is  believed  to  be  a  pulmonary  abscess  is  in 
reality  an  encapsulated  empyema  which  has  ruptured  into  a  bronchus 
(Fig.  337).  On  the  other  hand,  a  pulmonary  abscess  may  perforate  the 
visceral  layer  of  the  pleura.  The  pus  may  thus  become  encysted  and 
form  an  encapsulated  empyema. 

The  amount  of  pus  is  variable,  ranging  from  1  or  2  ounces  to  as  much 
as  2  pints. 

International  Clinics,  vol.  iv,  twenty-sixth  series. 


DISEASES    OF    THE    PLEURA 


555 


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expectoration.     Fever  of  the  type  usually  seen  in  septic  cases  is  usually 


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present  (Fig.  338).  This  is  especially  true  if  the  pus  is  located  between 
the  lung  and  diaphragm  or  between  the  visceral  and  parietal  layers  of 
the  pleura.  If  the  collection  of  pus  is  considerable  in  amount  the  con- 
stitutional symptoms  are  apt  to  be  marked. 


556  DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

If,  however,  the  pus  develops  between  the  lobar  fissures  and  is  small 
in  amount,  the  onset  may  be  frank  with  pain  and  fever  or  it  may  be 
insidious  and  the  symptoms  indefinite.  In  such  cases  the  picture  pre- 
sented is  suggestive  of  a  small  focus  of  suppuration,  namely,  fever,  with 
marked  remissions  or  intermissions,  anorexia,  and  malaise.  Pus  located 
between  the  fissures  acts  as  a  foreign  body  and  thus  produces  cough  and 
expectoration.  As  already  stated  the  first  intimation  of  the  trouble 
may  be  the  expectoration  of  a  considerable  amount  of  pus  as  the  result 
of  rupture  of  the  pus  into  a  bronchus. 

Physical  Signs. — Inspection.- — If  the  amount  of  pus  is  small  and  has 
been  present  only  for  a  short  time,  nothing  of  note  will  be  seen  on  in- 
spection. If,  on  the  other  hand,  it  has  been  present  for  some  time  it 
will  produce  much  the  same  effect  as  a  foreign  body.  Thus  the  surround- 
ing lung  tissue  may  be  congested,  atelectatic  or  even  fibroid  in  character. 
In  such  cases  there  will  be  more  or  less  restriction  of  expansion  on  the 
affected  side  and  in  addition  the  chest  wall  may  be  retracted. 

Palpation. — If  one  has  reason  to  suspect  that  an  encysted  empyema 
may  be  present  the  chest  should  be  palpated  by  means  of  firm  pressure 
with  the  finger  tips.  This  may  reveal  a  localized  area  of  edema  or  a 
sharply  circumscribed  area  of  tenderness.  The  latter  is  very  suggestive 
of  the  presence  of  localized  pus.  Tactile  fremitus  is  variable;  its  presence 
or  absence  will  depend  largely  on  the  size  of  the  effusion. 

Percussion. — This  should  be  performed  lightly  in  order  to  distinguish 
between  the  flatness  over  the  fluid  and  the  dulness  over  the  compressed 
lung  tissue  surrounding  the  fluid. 

Auscultation. — If  the  effusion  is  sufficiently  large,  there  may  be  a  slight 
area  over  the  fluid  and  about  this  broncho-vesicular  or  bronchial  breathing 
and  mixed  rales  over  the  collapsed  or  congested  lung.  In  the  same 
manner  the  voice  sounds  may  be  absent  at  one  point  and  slightly  increased 
in  others. 

Diagnosis. — When  all  is  said  and  done  the  recognition  of  an  encysted 
empyema  is  extremely  difficult.  The  history,  the  symptoms  and  the 
physical  signs  are  rarely  conclusive;  as  a  rule,  they  are  only  suggestive. 

Inasmuch  as  an  encysted  empyema  is  not  an  infrequent  sequel  of 
lobar  pneumonia  the  persistence  of  symptoms,  leucocytosis  and  physical 
signs  after  the  termination  of  an  attack  of  pneumonia  should  arouse 
suspicion  as  to  the  presence  of  loculated  pus.  I  have  emphasized  else- 
where the  fact  that  delayed  resolution  is  an  infrequent  termination  of 
pneumonia.  In  the  great  majority  of  cases  believed  to  be  due  to  delayed 
resolution,  the  actual  cause  of  the  failure  ofn  the  lung  to  return  to  its 
normal  state,  is  the  presence  of  pus  in  the  pleural  cavity.  The  pus  may 
be  free  or  encysted. 

The  development  of  pulmonary  symptoms  a  week  or  so  after  a  surgical 
operation  also  should  arouse  the  suspicion  that  pus  may  be  present  in  the 
chest.  This  is  especially  true  in  suppurative  conditions  involving  the 
abdominal  viscera. 

In  common  with  other  long-standing  pulmonary  infections  a  loculated 
empyema  is  very  frequently  mistaken  for  tuberculosis.  The  cough,  ex- 
pectoration, slight  fever,  and  malaise  are  very  suggestive  but  the  absence 
of  tubercle  bacilli  from  the  sputum  and  the  location  of  the  abnormal 
physical  signs  should  serve  to  eliminate  tuberculosis. 

The  exploring  needle  may  be  used  if  the  evidence  points  strongly  to 


DISEASES    OF   THE    PLEURA  557 

the  presence  of  fluid.  In  addition  every  case  with  respiratory  symptoms 
the  cause  of  which  is  obscure,  should  be  examined  by  means  of  the  X-rays. 
Exploratory  thoracotomy  has  been  so  perfected  that  the  operation  can 
be  performed  with  as  little  risk  as  an  abdominal  exploration.  It  should 
be  recommended,  therefore,  in  all  cases  whether  the  pus  is  definitely 
located  or  not. 

HEMORRHAGIC  PLEURAL  EFFUSIONS 

As  the  majority  of  pleural  effusions  are  inflammatory  in  origin  it  is  no 
unusual  occurrence  to  find  red  blood  cells  in  the  fluid.  In  the  great 
majority  of  instances  the  number  of  red  corpuscles  is  too  small  to  cause 
any  alteration  in  the  color  of  the  effusion.  Dieulafoy  as  the  result  of 
histological  studies  of  pleural  fluids,  found  that  the  presence  of  from 
1500  to  3000  red  cells  per  cubic  millimeter  caused  no  appreciable  altera- 
tion in  the  color  of  the  fluid.  If,  however,  the  number  of  red  corpuscles 
reaches  5000  or  6000  per  cubic  millimeter  a  rosy  tint  is  imparted  to  the 
fluid  and  the  higher  the  cell  content  the  more  markedly  hemorrhagic  does 
the  effusion  become.  A  curious  feature  of  hemorrhagic  effusions  is  the 
occasional  presence  of  an  excessive  number  of  eosinophiles  not  only  in  the 
fluid  itself  but  also  in  the  circulating  blood.  The  same  thing  has  been 
noted  in  cases  of  hemothorax.  Klein1  has  recorded  a  case  in  which  the 
pleural  fluid  showed  76.4  per  cent,  and  the  systemic  blood  40  per  cent, 
eosinophiles;  Dieulafoy's  case  had  35  per  cent,  in  the  effusion  and  10  per 
cent,  in  the  circulating  blood.  In  other  instances  an  excess  of  eosino- 
philes may  be  present  in  the  pleural  fluid  and  not  in  the  circulating  blood  and 
vice  versa.  Thus  Harmsen2  found  8.64  per  cent,  of  eosinophiles  in  the 
pleural  fluid  alone;  on  the  other  hand,  Lord  observed  a  case  in  which  there 
were  no  eosinophiles  in  the  effusion  but  20  per  cent,  of  the  white  cells  in 
the  circulating  blood  were  of  that  character. 

The  discovery  of  a  hemorrhagic  effusion  is  almost  invariably  an  acci- 
dental finding.  Occasionally  its  presence  may  be  suspected  when  an 
effusion  develops  in  an  individual  known  to  be  cancerous.  As  effusions 
which  develop  secondarily  to  malignant  disease  of  the  mediastinum,  lungs 
or  pleura  are  quite  as  often  serofibrinous  as  hemorrhagic  and  the  latter 
have  no  distinctive  signs,  it  can  be  seen  that  such  a  diagnosis  prior  to 
thoracentesis  is  nothing  more  than  a  guess.  A  hemorrhagic  effusion  is 
encountered  in  the  following  conditions:  1.  Tuberculosis.  This  is  prob- 
ably the  most  common  cause  of  blood-stained  effusions.  As  has  been 
pointed  out  in  the  section  on  pleurisy  the  first  manifestation  of  tubercu- 
losis may  be  a  pleural  effusion.  Rarely  the  effusion  is  hemorrhagic  in 
character.  It  is  the  result  of  a  primary  tuberculosis  of  the  pleura  or  the 
coincident  involvement  of  the  lung  and  overlying  pleura.  The  hemor- 
rhagic character  of  the  fluid  is  to  be  explained  by  the  congestion  which 
surrounds  the  newly  formed  tubercles  and  the  vascularity  of  the  new  tissue. 
Leakage  occurs  later  partly  as  the  result  of  degeneration  of  the  small  ves- 
sels and  partly  as  the  result  of  involvement  of  the  vessels  of  the  tuber- 
culous process. 

The  condition  is  analogous  to  an  hemoptysis  which  may  be  the  imme- 
diate forerunner  of  active  tuberculosis  or  there  may  be  an  indefinite  period 
of  latency.     As  an  early  manifestation  the  effusion  is  apt  to  occur  in 

1  Cent.  f.  innere  Med,,  Jan.  28,  1S<)<). 

2  Quoted  by  Klein. 


558         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

individuals  who  are  apparently  healthy.  An  excess  of  lymphocytes  in  the 
fluid  is  very  suggestive  of  tuberculosis.  In  any  case  the  sediment  from 
the  fluid  should  be  examined  for  the  presence  of  tubercle  bacilli  and  in 
their  absence  animal  inoculations  should  be  made. 

More  rarely  an  acute  miliary  tuberculosis  or  a  rapidly  advancing 
tuberculous  broncho-pneumonia  is  associated  with  an  effusion  which  is 
hemorrhagic  in  character.  This  is  also  to  be  ascribed  to  involvement  of 
the  pleura. 

Occasionally  blood-stained  effusions  are  encountered  in  the  ordinary 
chronic  type  of  tuberculosis.  The  reaccumulation  of  the  fluid  is  very 
common.  It  must  be  borne  in  mind,  however,  that  the  same  thing  is 
commonly  seen  in  malignant  disease  and  occasionally  in  hemorrhagic 
effusions  of  an  apparently  benign  origin.  Hemorrhagic  effusions, 
tuberculous  in  origin,  may,  after  several  tappings,  become  serous  in 
character. 

2.  Malignant  Disease. — This  is  a  well-recognized  cause  of  hemor- 
rhagic effusions.  In  individuals  who  are  known  to  be  suffering  from 
malignant  disease  in  some  portion  of  the  body  or  who  have  been  operated 
on  some  time  previously  for  a  malignant  tumor,  the  occurrence  of  a 
hemorrhagic  effusion  is  the  strongest  kind  of  evidence  that  metastasis  to 
the  thoracic  viscera  has  taken  place.  Such  cases  offer  little  difficulty. 
If,  however,  the  effusion  is  secondary  to  primary  malignant  disease  in  the 
mediastinum,  lungs  or  pleura  which,  as  yet,  has  given  no  evidence  of  its 
presence,  the  diagnosis  may  remain  doubtful  for  some  time.  Ross1  in 
60  cases  of  malignant  disease  involving  the  mediastinum  found  an  effusion 
in  29,  and  of  this  number  15  were  hemorrhagic.  Rapid  reaccumulation 
of  the  fluid  is  suggestive  of  both  tuberculosis  and  malignant  disease  and 
is  apt  to  be  more  persistent  in  the  latter.  Dieulafoy  records  a  case  in 
which  thoracentesis  was  performed  thirty-three  times  in  four  months,  and 
44  pints  of  hemorrhagic  fluid  withdrawn. 

Cytological  examination  of  the  fluid  will  show  the  absence  of  lympho- 
cytes and  tubercle  bacilli.  The  finding  of  large  masses  of  cells  or  the  so- 
called  cancer  cells  is  looked  upon  by  some  observers  as  strong  evidence 
of  the  presence  of  malignant  disease. 

3.  Asthenic  Conditions. — Occasionally  a  hemorrhagic  effusion  is 
encountered  in  association  with  conditions  characterized  by  marked 
asthenia.  Among  these  may  be  mentioned  the  malignant  types  of  the 
acute  infectious  fevers,  scurvy  and  occasionally,  the  transudates  occurring 
in  the  course  of  chronic  nephritis  and  cardiac  disease.  Pressure  on 
the  azygos  veins  is  also  given  as  a  rare  cause  of  a  hemorrhagic  transudate. 
Hemorrhagic  effusions  are  not  uncommon  in  association  with  cirrhosis 
of  the  liver  but  in  the  majority  of  these  cases  tuberculosis  is  also  present 
and  is  to  be  looked  upon  as  the  actual  cause. 

4.  Simple  or  Idiopathic  Cases. — Not  infrequently  a  hemorrhagic  effu- 
sion occurs  in  an  individual  in  whom  there  is  no  evidence  of  either  tuber- 
culosis or  malignant  disease.  Osier  refers  to  an  instance  in  which  the 
patient  was  entirely  well  eight  years  later  and  Cheesman  and  Ely2  have 
recorded  a  case  in  which  the  pleural  effusion  reaccumulated  for  a  period 
of  eighteen  months  and  the  peritoneal  fluid  for  nearly  five  years.  This 
patient  also  showed  no  evidence  of  either  tuberculosis  or  malignant 

1  Edinburgh  Med.  Jour.,  December,  1914. 

2  Am.  Jour.  Med.  Sc,  August,  1899. 


DISEASES    OF    THE    PLEURA  559 

disease.  These  are  exceptional  cases.  In  the  majority  of  instances 
these  idiopathic  cases  are  to  be  looked  upon  as  tuberculous  although  the 
interval  between  the  appearance  of  the  hemorrhagic  effusion  and  definite 
tuberculosis  may  be  a  long  one.  The  same  may  be  said  of  hematoma  of 
the  pleura  which  is  given  as  a  rare  cause  of  hemorrhagic  effusion. 

5.  Finally  mention  should  be  made  of  the  fact  that  in  performing  the 
operation  of  thoracentesis  a  small  vessel  may  be  punctured  and  blood 
in  this  way  may  become  mixed  with  a  serofibrinous  exudate.  A  rare 
accident  is  puncture  of  an  intercostal  artery  with  the  aspirating  needle. 
Death  resulted  from  this  accident  in  a  case  observed  by  Horder.1 

The  symptoms  and  physical  signs  are  the  same  as  those  occurring  in 
serous  effusions. 

HEMOTHORAX 

Etiology. — An  effusion  of  blood  into  the  pleural  cavity  may  occur  as 
the  result  of  rupture  of  an  intrathoracic  blood-vessel  or  of  an  intercostal 
artery.  The  latter  is  by  far  the  most  common.  There  are  two  groups 
of  cases:  the  non-traumatic  and  the  traumatic. 

1.  The  non-traumatic  cases  are  due  to  rupture  of  a  blood-vessel 
which  is,  as  a  rule,  diseased.  The  most  common  cause  is  aneurism. 
Occasionally  the  rupture  of  a  thoracic  aneurism  may  lead  to  the  escape 
of  an  enormous  quantity  of  blood  into  the  pleural  cavity.  When  rupture 
into  a  pleural  cavity  does  occur,  it  is  usually  on  the  left  side.  Among 
22  cases  collected  by  Goodman,2  rupture  into  the  left  pleural  cavity 
occurred  in  7,  while  the  right  side  was  involved  but  once.  Fowler  ob- 
served a  case  in  which  a  fatal  issue  occurred  as  the  result  of  rupture  of  a 
small  aneurism  of  one  of  the  internal  mammary  arteries.  Caries  of  one 
of  the  ribs  may  cause  erosion  of  an  intercostal  artery  followed  by  hemor- 
rhage into  the  pleural  cavity. 

Tumors  by  causing  pressure  on  the  larger  intrathoracic  veins,  may 
lead  to  the  establishment  of  a  collateral  circulation.  The  smaller  veins 
which  take  up  the  burden  of  the  circulation  may  become  greatly  dilated 
or  varicose  and  one  of  these  varicosities  may  rupture  (West) . 

Erosion  of  one  of  the  intrathoracic  vessels  by  cancer,  or  an  abscess, 
is  an  occasional  cause  of  hemorrhage.  Rarely  an  effusion  of  pure  blood 
into  the  pleural  cavity  occurs  in  cases  of  scurvy  and  hemophilia. 

2.  Traumatic  Hemothorax. — This  is  by  far  the  most  common 
variety.  Penetrating  wounds  of  the  chest  are  not  especially  common  in 
civil  life  but  in  military  practice  they  are  of  frequent  occurrence  and  a  very 
high  proportion  of  them  are  followed  by  a  hemothorax.  It  is  important  to 
bear  in  mind  that  the  bleeding  which  follows  a  penetrating  wound  of  the 
chest  does  not  come  from  the  perforated  lung  but  from  the  parietal  pleura. 
"When  we  consider  how  readily  the  intercostal  vessels  may  be  torn  by 
a  bullet  or  by  a  fragment  of  fractured  rib  projected  by  the  bullet,  this 
is  not  surprising"  (Keogh  Murphy).  It  is,  of  course,  understood  that  this 
applies  to  wounds  beyond  the  middle  line.  Perforation  of  the  large 
vessels  at  the  root  of  the  lung  or  a  great  vein  at  the  root  of  the  neck  may 
be  followed  by  a  rapid  and  fatal  hemorrhage  into  the  pleural  cavity. 

It  is  interesting  to  note  that  perforation  of  the  lung  itself  by  a  bullet 

Allbutt  and  Rolleston:  "System  of  Medicine,"  vol.  v,  p.  559. 
2  Jour.  Am.  Med.  Assoc,  April  18,  1914 


560  DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

of  small  caliber,  providing  the  main  vessels  escape,  is  not  attended  by 
hemorrhage.  As  Makins1  has  pointed  out,  there  is  no  reason  why  a 
perforation  by  a  bullet  of  small  caliber  should  be  much  more  feared  than 
a  puncture  from  an  exploring  trocar.  This  is  due  to  the  fact  that  the 
lung  is  composed  largely  of  elastic  tissue  which  at  once  contracts  closing 
up  the  hole  made  by  the  bullet;  at  the  same  time  the  contractile  power 
effectively  seals  up  the  opening  in  the  visceral  pleura.  Even  relatively 
large  vessels  and  bronchi  may  be  perforated  and  sealed  up  by  the  elastic 
tissue  surrounding  them.  Healing  of  the  pleural  surface  takes  place  with 
great  rapidity;  so  much  so  that,  within  three  or  four  days  of  the  injury, 
it  will  be  difficult  to  find  at  post-mortem  the  actual  track  of  the  bullet 
through  the  lung  (Murphy). 

In  Murphy's2  experience  penetrating  wounds  of  the  chest  are  compli- 
cated by  a  hemothorax  in  about  60  to  70  per  cent,  of  all  cases  as  the 
result  of  a  gradual  continued  oozing  from  an  intercostal  vessel.  The  fre- 
quency varies  enormously,  however,  with  the  early  treatment.  Pro- 
longed rest  immediately  after  the  injury  greatly  reduces  the  incidence. 
If  the  wounded  are  transported  some  distance  shortly  after  the  injury  is 
received  the  percentage  of  cases  developing  a  hemothorax  is  very  high. 
In  the  South  African  War,  Makins  pointed  out  that  among  the  men  who 
were  at  once  brought  to  a  base  hospital  and  kept  at  rest,  the  hemothorax 
occurred  in  30  per  cent,  but  in  those  who  were  transported  long  distances, 
hemothorax  occurred  in  no  less  than  90  per  cent,  of  all  penetrating  wounds 
of  the  chest.  Makins  divides  these  cases  into  the  following  groups: 
(1)  Gradual  or  primary  hemothorax  due  to  steady  small  oozing  from  the 
time  the  wound  was  received;  (2)  recurrent,  where  several  hemorrhages 
have  occurred;  (3)  secondary  hemorrhage  which  is  the  same  as  that  occur- 
ring elsewhere  and  apt  to  happen  somewhere  about  the  eighth  or  tenth 

The  relative  infrequency  of  penetrating  wounds  in  civil  life  and  the 
excellent  hospital  facilities  in  most  communities  explain  to  a  great  extent 
the  rarity  of  hemothorax  in  any  but  military  practice. 

Symptoms. — The  initial  symptoms  vary  with  the  nature  of  the  wound 
and  the  amount  of  bleeding.  The  rupture  of  a  thoracic  aneurism,  or 
opening  of  a  large  vessel  as  the  result  of  trauma,  is  followed  by  profound 
shock  and  death  within  a  few  minutes.  If  the  source  of  the  bleeding  is 
from  a  torn  intercostal  artery  the  early  symptoms  may  be  so  slight  as  to 
pass  unnoticed.  Usually,  however,  there  is  some  evidence  of  shock, 
especially  if  the  injury  occurs  in  the  lower  part  of  the  chest.  The  shock  is 
to  be  attributed  to  the  injury  of  the  chest  wall  and  the  thoracic  concussion 
rather  than  to  that  of  the  lung  itself.  The  patient  is  pale,  has  a  rapid 
and  weak  pulse  and  he  may  faint.  External  bleeding  is  usually  very 
slight  in  amount.  Pain  is  not  a  marked  feature,  especially  after  bullet 
wounds.  There  may  be  some  pain  and  tenderness,  however,  at  the  point 
of  entrance  and  exit,  especially  if  a  rib  has  been  fractured.  For  a  short 
time  after  receiving  the  wound  the  patient  feels  as  though  his  "wind  had 
been  knocked  out."  There  is  some  difficulty  in  getting  the  breath  and  a 
feeling  of  oppression  in  the  chest.  This,  however,  passes  off.  Hiccough 
and  vomiting  point  strongly  to  perforation  of  the  diaphragm. 

Hemoptysis  after  a  bullet  wound  is  not  uncommon.     Blood-streaked 

1  "Surgical  Experiences  in  South  Africa,  1899-1900." 

2  "Wounds  of  the  Thorax  in  War,"  1915. 


DISEASES    OF    THE    PLEURA  561 

sputum  may  be  present  for  three  or  four  days  and  then  suddenly  cease. 
Eloesser1  states  that  blood-streaked  sputum  is  not  always  an  evidence  of 
perforation  of  the  lung  as  it  may  follow  a  severe  contusion  of  the  chest 
wall.  If  the  bullet  does  not  pierce  a  large  vessel  or  injure  an  intercostal 
artery,  little  or  no  inconvenience  is  felt.  There  is  slight  tenderness 
at  the  point  of  entrance  and  exit,  difficulty  in  breathing  and  a  sense 
of  oppression  immediately  after  the  injury  and  possibly  some  blood- 
streaked  sputum  for  a  few  days.  At  the  end  of  this  time  the  individual 
is  again  ready  for  duty. 

If  the  hemorrhage  into  the  pleural  cavity  has  occurred,  there  is  apt  to 
be  some  fever  about  the  third  or  fourth  day.  The  temperature  is  irregu- 
lar and  if  recurrent  bleeding  takes  place  the  temperature  again  rises. 
Secondary  rises  in  the  temperature  are  not  always  due,  however,  to  fresh- 
bleeding;  they  may  be  caused  by  infection,  mention  of  which  will  be  made 
later. 

If  the  hemorrhage  is  severe  but  not  immediately  fatal,  the  skin  is 
blanched  and  clammy,  the  pulse  rate  rapid  and  the  temperature  is  raised 
and  irregular  in  character.  Murphy  states  that  unless  one  of  the  great 
vessels  is  pierced,  the  hemorrhage  following  chest  wounds  is  rarely  fatal 
as  the  pressure  of  the  distended  pleural  cavity  will  check  the  bleeding. 

The  tendency  of  the  effusions  is  toward  spontaneous  absorption  and 
recovery.  Hall2  states  that  after  a  few  days  small  clots  are  deposited  on 
the  pleura.  In  the  rest  of  the  effusion  clotting  is  not  so  complete  and  the 
fluid  resembles  unaltered  blood,  but  on  standing  blood  cells  and  a  fine 
clot  are  deposited  leaving  a  yellowish  or  " porter-like"  fluid.  If 
aspiration  is  delayed  for  three  or  four  weeks  sedimentation  may  take  place 
and  the  fluid  withdrawn  is  similar  to  serum.  Brick-red  colored,  grumous 
fluid  is  characteristic  of  infection  (Makins). 

After  gunshot  wounds,  infection  is  of  frequent  occurrence  and  unless  rec- 
ognized death  is  apt  to  ensue.  In  Bradford's3  experience  approximately 
25  per  cent,  of  the  cases  of  hemothorax  were  infected.  In  80  per  cent, 
of  these  cases  the  infection  was  carried  in  from  the  skin  or  clothing;  in  the 
remaining  20  per  cent,  the  infection'  was  caused  by  organisms  derived 
from  the  lung.  When  infection  has  occurred,  the  symptoms  are  usually 
severe.  The  fever  is  higher,  the  pulse  rate  rapid,  dyspnea  becomes 
marked  and  the  skin  is  slightly  jaundiced.  It  is  important  to  keep  in 
mind  that  these  symptoms  may  appear  suddenly.  In  the  early  days  of 
the  European  war  the  symptoms  were  believed  to  be  due  to  secondary 
hemorrhage  but  post-mortem  examinations  showed  that  infection  of  the 
hemothorax  had  occurred.  The  appearance  of  such  symptoms  calls  for 
an  exploratory  puncture  and  if  infection  has  taken  place  the  pleura  should 
be  opened  and  drained  at  once.  Bradford  calls  attention  to  another 
group  of  cases  in  which  infection  with  anaerobic  gas-producing  organisms 
produces  characteristic  physical  signs  (see  below). 

Physical  Signs. — Inspection. — When  hemorrhage  has  taken  place 
into  the  pleural  cavity  the  affected  side  shows  more  or  less  bulging  at  the 
base  and  motion  is  much  restricted.  The  apex  beat  of  the  heart  may  be 
displaced  if  the  effusion  is  sufficiently  large.  If  the  effusion  has  become 
infected  with  a  gas-producing  organism,  the  heart  is  rapidly  displaced. 

1  Jour.  Am.  Med.  Assoc,  Dec.  4,  1915. 

2  "Surgery  in  War,"  1916. 

3  Lancet,  Jan.  29,  1916. 


562         DISEASES    OF    THE   BEOXCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Palpation. — Tactile  fremitus  is  absent. 

Percussion. — The  percussion  note  is  absolutely  dull.  Even  a  thin 
film  of  coagulated  blood  will  so  muffle  the  pulmonary  resonance  as  to  give 
the  impression  that  a  much  larger  effusion  is  present.  In  cases  infected 
with  the  gas  bacillus  a  "  cracked-pot "  percussion  note  is  frequently 
present  on  the  affected  side.  The  frequency  with  which  this  sign  occurs 
in  these  cases  is  considered  by  Bradford  to  be  almost  pathognomonic. 
As  the  coin  test  is  also  present  the  error  of  considering  the  condition  a 
pneumothorax  is  not  uncommon. 

Auscultation. — The  breath  sounds  are  either  absent  or  very  distant 
over  the  effusion.  Occasionally  the  breath  sounds  have  a  bronchial 
quality.  Over  the  upper  limits  of  the  effusion  egophony  may  be  heard, 
while  over  the  effusion  itself  the  voice  sounds  are,  as  a  rule,  faint  and 
distant  in  character.     There  are  no  rales  or  friction  rubs  to  be  heard. 

Abnormal  physical  signs  are  apt  to  persist  for  months  and  there  may  be 
permanent  alterations  on  the  affected  side.  The  chest  is  apt  to  show 
retraction,  the  respiratory  movement  is  greatly  diminished  and  the 
breath  and  voice  sounds  are  distant  or  absent. 

Diagnosis. — The  development  of  an  effusion  very  quickly  after  the 
receipt  of  an  injury  to  the  chest  is  almost  certainly  due  to  hemorrhage. 
In  the  non-traumatic  cases  the  presence  of  hemothorax  may  be  suspected 
if  it  is  known  that  the  patient  is  suffering  from  an  aneurism  or  caries  of 
the  rib.  The  only  other  condition  whiqh  occurs  so  quickly  is  a  pneumo- 
thorax the  physical  signs  of  which  are  entirely  different. 

Hall  states  that  considerable  consolidation  sometimes  takes  place  as 
the  result  of  infection  along  the  course  of  the  bullet  wound.  The  physical 
signs  consist  of  dulness,  lobar  in  distribution;  distant  bronchial  breathing 
and  fine  rales. 

CHYLOTHORAX 

The  presence  of  a  milky  or  lactescent  fluid  in  the  pleural  or  peritoneal 
cavity  is  not  a  common  event.  The  discovery  is  nearly  always  accidental 
and,  as  a  rule,  follows  the  tapping  of  one  of  these  cavities  for  what  is 
believed  to  be  an  ordinary  serous  effusion.  Three  types  of  milky -like 
fluid  are  to  be  distinguished:  chylous,  chyliform  and  pseudo-chylous. 
Shaw1  collected  from  the  literature  54  instances  of  milky  effusions,  of 
which  31  were  chylous,  13  chyliform  and  10  a  milky  effusion  of  doubtful 
nature. 

1.  Chylous  Fluid. — This  condition  most  commonly  follows  a  trauma 
in  which  the  thoracic  duct  has  been  ruptured.  One-third  of  the  cases 
have  been  attributed  to  this  cause.  It  may  result  also  from  anything 
which  causes  obstruction  to  the  lymph  flow  either  in  the  thoracic  duct  or 
large  lymphatic  vessels.  Among  these  causes  may  be  mentioned  throm- 
bosis of  the  left  subclavian  vein  and  malignant  disease  of  the  pleura, 
mediastinal  lymph  nodes  or  lymphatics.  Chylous  effusions  have  been 
encountered  also  in  cases  of  filariasis.  As  a  rule,  the  effusion  is  unilateral 
but  it  may  be  bilateral  and  in  some  instances  the  effusion  is  chylous  on 
one  side  and  serous  on  the  other.  In  the  majority  of  cases  a  chylous  effu- 
sion is  also  present  in  the  peritoneal  cavity. 

The  fluid  is  usually  white  and  milky  in  appearance.  In  some  instances 
it  has  a  pinkish  or  rosy  color  due  to  the  presence  of  a  small  amount  of 
1  Jour.  Pathology  and  Bacteriology,  1900,  vi,  p.  339. 


DISEASES    OF    THE    PLEURA  563 

blood.  More  rarely  the  fluid  may  have  a  yellowish  or  greenish  tint, 
giving  it  the  appearance  of  a  purulent  effusion.  It  is  possible  that,  in 
some  instances,  a  true  chylous  effusion  has  been  mistaken  for  purulent 
fluid.  On  standing  a  cream}'  layer  forms  on  the  top  but  the  fluid  retains 
its  milky  appearance.  The  fluid  is  resistant  against  putrefaction. 
Microscopically  the  fat  is  seen  to  consist  of  minute  globules.  Examined 
chemically  the  percentage  of  fat  is  found  to  be  0.5  per  cent,  or  less.  Sugar 
and  diastatic  enzymes  are  frequently  present. 

2.  Chyliform  Fluid. — Although  far  from  being  common  chyliform 
effusions  are  much  more  frequently  encountered  than  the  pure  chylous. 
In  the  great  majority  of  instances  chyliform  effusions  are  associated  with 
tuberculosis  or  malignant  disease,  especially  the  former.  An  effusion  of 
this  character,  may  be  extremely  chronic  and  usually  develops  insidiously. 
It  is  apt  to  first  manifest  itself  by  gradually  increasing  dyspnea.  Rarely 
the  onset  is  accompanied  by  pain  in  the  chest.  As  the  effusion  gradually 
increases  in  size  there  is  often  a  sense  of  oppression  in  the  chest  which  is 
at  once  relieved  by  tapping.  A  marked  feature  of  these  effusions  is  the 
tendency  to  recur.  This  is  quite  characteristic  of  effusions  due  to  malig- 
nant disease  of  the  pleura  and,  at  times,  in  those  which  are  tuberculous 
in  origin. 

Chyliform  fluid  is  odorless,  does  not  coagulate  on  standing  and  will 
keep  for  weeks  without  undergoing  putrefactive  changes.  The  color  is 
milky  but  at  times  may  have  a  pinkish  or  rosy  tint  due  to  the  admixture 
of  small  amounts  of  blood.  The  milky  appearance  of  chyliform  fluid 
is  due  to  the  presence  of  fat  liberated  by  the  breaking  down  of  leukocytes 
and  endothelial  cells  which  have  undergone  fatty  degeneration.  Quincke1 
in  1875,  was  the  first  to  point  out  that  there  were  two  types:  (1)  those  due 
to  pure  chylous  fluid  (Irydrops  chylosus),  and  (2)  those  due  to  cells  which 
had  undergone  f  atty  degeneration  (hydrops  chylif  ormis  seu  acliposus) .  The 
chyliform  fluid  is  to  be  distinguished  from  the  true  chylous  by  the  rela- 
tively high  fat  percentage.  The  fat  content  in  the  former  may  be  as 
high  as  6  per  cent,  compared  with  0.5  per  cent,  or  less,  in  the  latter 
(Adami  and  Xicholls).  Microscopically  the  fat  globules  are  much  larger 
and  in  addition  there  are  numerous  cells  in  different  stages  of  disintegration. 

3.  Pseudo-chylous  Fluid. — The  fluid  of  pseudo-chylous  effusions  is 
opaque  and  closely  resembles  diluted  skimmed  milk.  The  degree  of 
opacity  often  varies  considerably  at  different  tappings.  The  fluid  may 
have  a  pinkish  tint.  After  standing  for  some  time  it  appears  greenish 
by  reflected  light  and  a  membrane  forms  on  the  surface.  The  remark- 
able resistance  of  the  fluid  to  putrefactive  changes  may  be  due  to  two 
factors:  (1)  the  formation  of  a  membrane  on  the  surface;  or  (2)  to  the 
presence  of  lecithin.     The  specific  gravity  is  low. 

Pseudo-chylous  effusions  have  been  noted  in  association  with  cardiac 
disease,  amyloid  disease,  cirrhosis  of  the  liver  and  nephritis.  In  many 
cases  there  is  no  adequate  explanation.  Recently  attention  lias  been 
directed  to  the  occurrence  of  pseudo-chylous  effusions  associated  with 
nephritis,  probably  syphilitic  in  origin.  Cases  of  this  nature  have  been 
reported  by  Shaw,2  Weber3  and  Weber  and  Schmidt.4 

1  Deut.  Arch.  f.  Klin.  Med.,  Bd.  xvi,  1875,  p.  121. 

2  Proc.  Roy.  Soc.  Med.,  Clinical  Section,  1911,  iv,  112. 
*  Edinburgh  Med.  Soc.,  1913,  x,  348. 

4  International  Clinics,  vol.  i,  1916. 


564  DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

The  milky  appearance  of  pseudo-chylous  effusions  is  not  due  to  the 
presence  of  fat.  Joachim1  ascribed  it  to  a  pseudo-globulin.  According 
to  Wallis  and  Scholberg2  it  is  caused  by  a  lecithin-globulin  complex 
which  is  held  in  suspension  by  the  inorganic  salts  present.  Removal  of 
the  inorganic  salts  by  dialysis  results  in  the  precipitation  of  the  lecithin- 
globulin  and  the  disappearance  of  the  opalescence.  The  milky  appear- 
ance is  not  due  to  free  lecithin,  fat,  or  a  mucinoid  substance. 

Rarely  the  blood  serum  also  presents  a  milky  appearance.  Oswald3 
states  that  formerly  when  venesection  was  a  common  practice,  the  oc- 
casional occurrence  of  milky-looking  blood  serum  was  noted  but  never 
in  association  with  pseudo-chylous  effusions.  The  case  reported  by 
Weber  and  Schmidt  is  unique  by  reason  of  the  fact  that  the  blood  serum, 
which  at  first  was  normal  in  appearance,  became  milky  when  the  ascites 
and  pleural  effusion  were  rapidly  being  absorbed.  An  unusual  instance 
of  milky-like  effusion  has  been  recorded  by  West4  in  which  the  opales- 
cence was  caused  by  the  presence  of  calcium  phosphate. 

As  already  stated  the  discovery  of  a  milky  effusion  is  almost  invariably 
accidental  as  the  symptoms  and  physical  signs  are  those  of  an  ordinary 
effusion.  The  cause  of  the  opalescence  may  be  determined  partly  by 
microscopical  and  partly  by  chemical  examinations. 

HYDROTHORAX 

Etiology. — By  hydrothorax  is  meant  an  accumulation  of  clear  serous 
fluid  in  the  pleural  cavity.  It  is  a  transudate  and  non-inflammatory  in 
character  in  contradistinction  to  that  encountered  in  pleural  effusion 
which  is  an  exudate  and  inflammatory  in  origin.  Being  one  of  the  mani- 
festations of  a  general  dropsy,  it  occurs  in  a  number  of  conditions,  of  which 
chronic  valvular  heart  disease  and  nephritis  are  the  most  common. 
Hydrothorax  may  occur  also  as  the  result  of  a  hydremic  condition  of  the 
blood  of  local  stasis,  or  as  a  complication  of  a  mediastinal  growth,  a 
thoracic  aneurism  or  cirrhosis  of  the  liver. 

Morbid  Anatomy. — In  renal  cases  the  effusion  is  usually  bilateral, 
but  if,  as  often  happens,  the  heart  is  insufficient,  the  effusion  may  be 
unilateral  and  right-sided,  or  if  bilateral  there  will  be  an  excess  on  the 
right.  In  cardiac  affections  the  effusion  is  so  commonly  right-sided  or 
if  bilateral,  larger  on  the  right  side,  that  it  has  been  for  years  a  subject 
for  speculation  (Fig.  339).  Hydrothorax  is  also  apt  to  be  one-sided  in 
cases  of  mediastinal  growth  and  aneurism. 

The  hydrothorax  that  accompanies  heart  disease  has  been  recognized 
for  many  years.  Why  it  occurs  in  some  cases  and  not  in  others  is  not 
clear,  for  it  is  certain,  as  both  Flint  and  Da  Costa  long  since  remarked, 
that  the  phenomenon  bears  no  constant  relation  to  the  extent  of  the 
cardiac  disease.  "Not  only  are  these  lesions  (cardiac)  marked  in  cases 
in  which  dropsy  has  not  occurred,  but  dropsy  occurs  in  other  cases  in 
which  the  lesions  are  comparatively  slight"  (Flint). 

The  most  interesting  feature  of  cardiac  hydrothorax  is  that  the  effu- 
sion in  the  majority  of  cases  is  limited  to  the  right  side  or  if  bilateral 

1  Munch,  med.  Woch.,  1903,  1,  p.  1915. 

2  Quarterly  Jour.  Med.,  1910,  iii,  301. 

3  "Lehrbuch  der  chemischen  Pathologie,"  1907. 

4  Trans.  Clin.  Soc,  London,  1906,  xxxix,  42. 


DISEASES    OF    THE    PLEURA 


565 


that  on  the  right  is  by  far  the  largest.  While  it  is  quite  possible  that  no 
single  factor  is  responsible  for  this  peculiarity  it  is  certain  that  the  pre- 
dominance of  right-sided  accumulations  is  too  constant  to  be  accidental. 
This  has  long  been  appreciated  and  as  far  back  as  1863  Baccelli  offered  the 
theory  that  the  enlarged  heart,  by  dragging  the  superior  vena  cava  down- 
ward carried  with  it  the  vena  azygos  major  thus  drawing  it  tightly 
around  the  root  of  the  lung  and  causing  it  to  be  compressed.     More 


Fig.  339. — Right-sided  hydrothorax.     Atelectasis  of  lung.     Dilatation  of  left  auricle. 

recently  Steele  and  Stengel  championed  the  hypothesis  that  compres- 
sion of  the  azygos  vein  was  effected  by  extension  upward  of  the  dilated 
right  heart.  Largely  as  a  result  of  these  contributions  the  azygos- vein 
hypothesis  has  been  accepted  as  the  true  explanation. 

As  the  result  of  an  anatomical  study  of  this  phenomenon  Fetterolf  and 
I1  concluded  that  the  azygos  vein  hypothesis  was  untenable  for  the  fol- 
lowing reasons:  (1)  Only  about  two-thirds  of  the  parietal  membrane  is 
drained  by  the  azygos  vein;  (2)  the  collateral  anastomoses  of  the  azygos 
i  Fetterolf  and  Landis:  Am.  Jour.  Med.  Sc,  November,  1909. 


566  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

veins  are  so  free  and  so  numerous  that,  in  the  event  of  pressure,  competent 
bypaths  would  soon  be  established  and  carry  away  any  excess  of  fluid 
in  the  azygos  radicles;  (3)  the  vena  azygos  minor,  emptying  into  the  major, 
is  subject  to  the  same  influences  as  the  latter,  and  therefore  the  effusion 
should  always  be  bilateral;  (4)  it  is  anatomically  impossible  for  the  heart, 
either  directly  or  indirectly,  to  exert  pressure  upon  the  azygos  major 
vein;  (5)  it  does  not  explain  purely  left-sided  effusions. 

While  dilatation  of  the  right  auricle  is  the  deciding  factor  in  the  right- 
sided  effusions  we  found  that  the  pressure  was  exerted,  not  on  the  azygos 
vein,  but  on  the  pulmonary  veins  at  the  root  of  the  lung.  Confirmation 
of  this  assumption  is  found  in  the  fact  that  Miller1  has  shown  that  "the 
capillary  network  into  which  the  bronchial  artery  breaks  up  in  the 
(visceral)  pleura  gives  rise  to  radicles  which  join  the  pulmonary  vein." 
Therefore,  any  obstruction  of  the  pulmonary  veins  of  sufficient  duration 
and  if  accompanied  by  whatever  condition  of  the  blood  essential  to  transu- 
dation, would  cause  a  leakage  through  the  visceral  pleura  into  the 
pleural  sac.  Furthermore,  the  source  of  the  pleural  fluid  would  indicate 
that  a  similar  leakage  would  take  place  into  the  lung  itself;  and  of  this 
fact  there  is  clinical  evidence  that  such  is  the  case.  West  states  that  the 
obstruction  leads  to  edema  of  the  lung  rather  than  to  an  effusion  but  that 
the  two  conditions  are  frequently  associated.  Fowler  also  states  that  in 
cases  of  general  anasarca,  in  which  unilateral  pleural  adhesions  are  present, 
the  corresponding  lung  may  be  edematous  while  a  considerable  quantity 
of  fluid  may  be  found  in  the  opposite  pleura.  On  several  occasions  I 
have  noted  the  coexistence  of  an  effusion  and  small  moist  rales  in  the  lung. 

When  the  effusion  occurs  on  the  left  side  the  mechanism  is  much  the 
same  except  that  the  left  auricle  and  ventricle  are  dilated.  That  the 
left-sided  effusions  are  less  frequent  and,  when  present,  smaller  in  size, 
is  to  be  explained  by  the  fact  that  left-sided  dilatation  is  less  frequent  and 
also  because  pressure  effects  are  less  readily  exerted  on  the  left  pulmonary 
veins. 

The  occurrence  of  a  unilateral  effusion  as  the  result  of  a  thoracic 
aneurism  or  mediastinal  growth  may  be  brought  about  in  the  same 
manner. 

If  a  hydrothorax  has  been  present  but  a  short  time  the  pleural  sur- 
faces show  no  change  from  the  normal  but  if  of  long  standing  a  grayish 
deposit  may  be  noted  over  the  parietal  pleura.  This  can  be  scraped  off 
readily. 

The  lung  is  collapsed  but,  as  a  rule,  is  readily  reexpanded  on  removal 
of  the  fluid  (see  Fig.  340).  The  heart  as  in  effusions  from  other  sources 
is  displaced  if  the  effusion  is  sufficiently  large  (see  Figs.  109  and  206). 

Symptoms. — Inasmuch  as  hydrothorax  invariably  complicates  an 
illness  which  is  of  a  serious  nature,  and  which  is  characterized  by  well- 
marked  symptoms,  its  presence  is  often  masked.  It  is  a  notorious  fact 
that  effusions  of  this  character  are  detected  in  the  post-mortem  room  far 
more  often  than  during  life.  Distressing  dyspnea  is  so  often  a  promi- 
nent feature  in  cases  of  failing  compensation  that  the  possibility  of  its 
being  aggravated  by  or  being  entirely  due  to  a  pleural  effusion  is  often 
lost  sight  of.  It  should  be  a  fixed  rule  in  cardiac  and  renal  cases,  to  make 
a  careful  examination  of  the  chest  whenever  the  breathing  becomes  em- 
barrassed; whenever  there  is  a  sense  of  oppression;  or  whenever  the  pa- 

1  Am.  Jour.  Anat.,  vii,  404. 


DISEASES    OP    THE    PLEURA 


567 


tient  becomes  cyanosed.  Of  the  various  cardiac  affections  which  may  be 
complicated  by  an  effusion,  mitral  stenosis  seems  to  be  the  most  frequent 
cause.  It  is  of  the  utmost  importance  that  the  fluid  be  removed  as  it 
often  accumulates  with  great  rapidity  and  of  itself  may  be  the  cause  of  a 
fatal  termination.  In  any  case  withdrawal  of  the  fluid  affords  great 
relief. 


L  Fia.  340.— Atelectasis  in  a  case  of  hydro  thorax.  The  apex  of  the  lung  is  adherent  to  the 
parietal  pleura  as  was  also  the  anterior  surface  of  the  upper  lobe  at  the  point  at  which  a 
dense  fibrous  scar  is  seen.  The  pleural  cavity  was  filled  with  frozen  serum  which  was  re- 
moved. The  pericardial  sac  is  seen  in  front  of  the  retracted  and  compressed  lung  *  rom  a 
syphilitic  to  which  infection  the  scar  is  probably  due,  there  being  no  evidences  of  tuberculosis. 


Physical  Signs.— The  physical  findings  in  cases  of  hydrothorax  are 

the  same  as  those  occurring  in  the  ordinary  pleural  effusion.  The  one 
peculiarity  of  this  type  of  effusion  is  that  it  is  bilateral  in  about  one-third 
of  the  cases.  This  must  be  borne  in  mind  when  comparing  the  two  sides 
of  the  chest. 


568         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

PNEUMOTHORAX 

While  the  term  "pneumothorax"  implies  the  presence  of  air  or  gas  in 
the  pleural  cavity  the  occurrence  of  either  alone,  for  any  length  of  time, 
is  rare.  In  the'vast  majority  of  cases  there  is  in  addition  to  the  air  or  gas 
a  serous  or  purulent  effusion,  hence  the  prefixes  hydro  or  pyo  to  denote 
one  or  the  other  of  these  composite  conditions.  Even  in  cases  in  which 
nitrogen  gas  is  introduced  into  the  pleural  cavity  for  therapeutic  purposes 
the  resulting  pneumothorax  becomes  a  hydropneumothorax  in  about  50 
per  cent,  of  the  cases.  Occasionally  a  pyopneumothorax  results  from  this 
procedure;  two  such  accidents  have  occurred  at  the  Phipps  Institute. 

Etiology. — As  an  exciting  cause  of  pneumothorax  -pulmonary  tubercu- 
losis easily  stands  first.  One  is  not  overestimating  its  importance  in  this 
connection  in  asserting  that  not  less  than  30  per  cent,  of  all  pneumotho- 
races  are  associated  with  tuberculosis  of  the  lungs.  As  a  complication  of 
pulmonary  tuberculosis  pneumothorax  can  be  expected  in  about  5  per 
cent,  of  all  cases.  A  pneumothorax  may  arise  also  as  the  result  of  other 
pulmonary  lesions,  namely,  gangrene,  abscess,  bronchiectasis,  hemorrhagic 
infarct,  the  rupture  of  an  emphysematous  bleb,  etc.  Occasionally  the 
pneumothorax  is  produced  by  an  empyema  rupturing  into  the  lung  and 
thus  allowing  the  escape  of  air  into  the  pleural  cavity. 

In  rare  instances  a  pneumothorax  is  produced  as  the  result  of  the  ex- 
tension of  a  lesion  in  some  neighboring  organ  as,  for  instance,  carcinoma  of 
the  stomach  or  esophagus  or  abscess  of  the  liver. 

Perforating  wounds  of  the  chest  wall  may  also  cause  a  pneumo-  or 
hemopneumothorax.  Finally  a  hydro-  or  pyothorax  may  be  changed  into 
a  hydro-  or  pyopneumothorax  as  the  result  of  the  introduction  of  air  into 
the  pleural  cavity  during  the  operation  of  paracentesis.  Under  these 
circumstances  it  is  probably  caused  by  faulty  technique. 

The  condition  occurs  more  frequently  in  males  than  females,  probably 
because  most  of  the  statistical  studies  deal  with  hospital  cases  among 
which  the  males  always  predominate.  It  is  almost  invariably  encoun- 
tered in  the  earlier  periods  of  life  as  is  to  be  expected  from  its  frequent 
association  with  fatal  cases  of  tuberculosis. 

Now  and  then  one  encounters  an  instance  of  so-called  spontaneous 
pneumothorax  in  which  the  accident  occurs  in  an  apparently  healthy 
individual  and  without  gross  disease  of  the  lungs.     Recovery  is  the  rule. 

Morbid  Anatomy. — In  order  to  appreciate  the  nature  of  this  accident 
a  knowledge  of  the  physics  of  the  chest  is  essential  (see  Fig.  94).  "The 
whole  outer  surface  of  both  elastic  lungs  is,  by  means  of  its  smooth, 
moist  covering  of  pleura,  intimately  and  hermetically  applied  to  the 
inner  surface  of  the  chest  wall,  which  in  its  turn  is  covered  by  the  parietal 
pleura.  By  reason  of  their  complete  elasticity  the  lungs  are  able  to 
follow  every  change  in  the  capacity  of  the  thorax,  without  causing  the  two 
layers  of  the  pleura  ever  to  separate.  The  cavity  of  the  unexpanded 
thorax  is  greater  than  the  volume  of  the  collapsed  lungs  when  removed 
from  the  body;  therefore,  the  lungs  in  their  natural  position  within  the 
chest  must  be  stretched,  and  they  are,  to  a  certain  degree,  in  a  state  of 
elastic  tension.  This  tension  varies  directly  with  the  size  of  the  thoracic 
cavity.  If  the  pleural  cavity  be  opened  by  a  perforation  from  without  or 
by  a  wound  of  the  lungs  from  within,  the  elasticity  of  the  lungs  causes 
them  to  collapse,  and  there  arises  an  air  space  between  the  outer  surface 


DISEASES    OF    THE    PLEtRA  569 

of  the  lungs  and  the  inner  surface  of  the  thorax  "  (Landois) .  Furthermore, 
it  is  to  be  borne  in  mind  that  under  normal  conditions  there  is  a  negative 
pressure  in  the  pleural  cavity  amounting  to  about  6  mm.  of  Hg.  If,  how- 
ever, the  outside  air  enters  the  pleural  cavity,  either  as  a  result  of  rupture 
of  the  lung  or  perforation  of  the  chest  wall,  the  normal  negative  pressure 
approaches  zero  and  as  the  air  accumulates  in  the  cavity  the  pressure  be- 
comes positive  instead  of  negative.  It  is  because  of  this  elastic  tension  of 
the  lungs  that  the  heart,  which  is  more  or  less  movable,  is  held  in  its  nor- 
mal position.  If,  however,  one  of  these  elastic  bands  is  severed,  as  in 
the  case  of  pneumothorax,  the  displacement  of  the  heart  toward  the.  un- 
affected side  is  immediate  and  often  attended  with  considerable  shock. 
Later,  as  the  air  accumulates  under  pressure  or  an  effusion  develops,  the 
displacement  of  the  heart  may  be  increased  as  the  result  of  pressure. 

Inasmuch  as  pneumothorax  is  most  commonly  encountered  as  a  com- 
plication of  pulmonary  tuberculosis  its  development  under  these  circum- 
stances will  be  considered  in  detail.  In  considering  the  pathology  of 
pulmonary  tuberculosis  and  of  pleurisy  complicating  that  disease  it  was 
shown  that  one  of  the  first  results  of  the  tuberculous  process  was  an  in- 
flammatory reaction  in  the  overhung  pleura  which  resulted  in  the  two 
layers  of  the  pleura  becoming  adherent.  The  older  the  tuberculosis  the 
more  dense,  as  a  rule,  is  the  thickening  of  the  adjacent  pleura.  Without 
obliteration  of  the  pleural  cavity  over  the  diseased  area  pneumothorax 
would  occur,  in  all  probability,  in  a  large  number  of  cases  of  tuberculosis 
instead  of  being  encountered  in  relatively  few. 

In  order  to  bring  about  the  accident  it  is  essential  that  the  pleural 
layers  are  not  adherent  or  if  they  are,  that  the  adhesions  are  slight  and 
easily  separated.  Another  requisite  is  the  formation  of  a  caseous  area 
just  beneath  the  visceral  layer,  which  constitutes  the  point  of  weakness. 
The  leak  may  occur  as  the  result  of  ulceration  through  the  intervening 
barrier  or  a  rupture  of  the  weakened  point  may  be  produced  by  some 
unusual  inspiratory  strain,  such  as  a  parox}rsm  of  coughing  or  severe 
exertion. 

The  occurrence  of  a  pneumothorax  is  always  possible  in  acutely  ad- 
vancing tuberculosis  of  the  lungs  because  the  disease  may  spread  to  the 
periphery  so  rapidly  that  the  pleural  surfaces  have  not  had  time  to  become 
firmly  adherent.  In  the  chronic  advanced  cases  rupture  of  the  lung 
rarely  occurs  over  the  site  of  the  oldest  disease  at  the  apex  but,  as  a  rule,  in 
the  lower  part  of  the  lung  more  recently  involved.  For  the  same  reason 
the  pneumothorax  may  occur  in  the  lung  secondarily  involved  because  the 
disease  is  more  recent  and  the  pleural  surfaces  are  not  so  firmly  adherent. 
In  some  series  of  cases  the  largest  proportion  of  cases  have  occurred  on  the 
right  side;  in  others  the  difference  between  the  two  sides  was  not  marked. 

In  the  majority  of  the  cases  the  accident  is  encountered  in  the  moder- 
ately advanced  and  advanced  cases  of  tuberculosis,  the  rupture  occurring 
in  the  lateral  portion  of  the  upper  lobe  between  the  third  and  sixth  ribs. 
Occasionally,  however,  it  is  met  with  in  incipient  cases  in  which  the 
initial  lesion  has  been  situated  close  to  the  periphery  of  the  lung  or  lias 
extended  to  that  location  very  rapidly  and  without  producing  oblitera- 
tion of  the  overlying  pleural  space. 

As  a  rule  there  is  but  one  point  of  rupture  two  or  more  openings  may 
be  present,  however.  The  opening  may  remain  patulous.  If  i1  does  the 
intrapleural  pressure  will  be  found  to  be  zero.     In  most  instances  the 


570         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

tissues  in  the  immediate  vicinity  of  the  perforation  act  like  a  valve  which 
permits  the  air  to  enter  the  pleural  cavity  during  inspiration  and  as  the 
respiratory  movement  is  reversed,  the  valve  closes  so  that  no  air  can 
escape; "as  a  result,  air  accumulates  in  the  pleural  cavity  under  pressure. 
Unless  death  takes  place  at  once  or  within  a  day  or  so,  fluid  develops. 


Expansion  1 
— ,  inter- 

spaces  full. 

v.  fremitus 

O.  v.  reso- 
nance O 

percussion 
flat.  Breath 

sounds  O 


No  phrenic 
wave. 


f  Expansion 
+  .  v.  frem- 
itus +  .  v. 
resonance 
+  .   Percus- 
sion: 
hyper- 
resonant. 
Breath 
sounds: 
exagger- 
ated. 


V.  fremitus 
+  +.▼- 

|  resonance 
+  ,  Percus- 
sion: slight 
dulness , 
Breath 
sounds: 
broncho- 
vesicular 


Phrenic 
wave  +. 


Fig.  341. — Pneumothorax  with  complete  collapse  of  the  right  lung. 

This  may  be  serous  in  the  beginning,  but  in  cases  of  advanced  tuberculosis 
it  soon  becomes  purulent. 

With  the  development  of  the  effusion  and  especially  if  the  air  accumu- 
lates under  pressure,  the  primary  displacement  of  the  heart  is  increased 
and  if  the  right  side  is  involved  the  liver  is  pushed  down.     The  displace- 


DISEASES    OF   THE    PLEURA 


571 


ment  of  the  liver  depends  in  part  on  the  weight  of  the  fluid  and  in  part  to 
the  alteration  of  the  intrapleural  pressure. 

When  perforation  of  the  lung  occurs  the  pneumothorax  may  be  com- 
plete or  partial.  When  complete,  the  entire  lung  is  collapsed  and  occu- 
pies the  same  position  as  in  cases  of  pleural  effusion,  namely,  the  upper 
and  inner  portion  of  the  chest  cavity  along  the  spinal  gutter  (Fig.  341). 

As  the  result  of  dense  pleuritic  adhesions  the  pneumothorax  maybe 
partial  in  character.  Thus  only  the  lower  lobe  may  be  collapsed  (Fig. 
342)  or  the  air  may  be  limited  to  the  antero-lateral  or  postero-lateral 
regions  (see  Fig.  345),  or  it  may  be  located  in  the  mid-lateral  region. 
Rarely  it  is  limited  to  the  superior  portion  of  the  chest. 


Fig.  342. — Large  cavity  occupying  upper  half  of  lung.  Perforation  into  the  pleural 
cavity  occurred.  The  thickened  anterior  portion  of  the  pleura  is  reflected  to  show  the 
localized  pyopneumothorax.     (Jefferson  Medical  College  Museum.) 

The  circumstances  under  which  pneumothorax  develops  as  a  compli- 
cation of  other  acute  or  chronic  inflammatory  affections  of  the  lungs  or 
of.'disease  in  adjacent  organs  do  not  require  further  notice.  Just  as  in 
the  case  of  tuberculosis,  if  the  pleural  space  overlying  the  pulmonary 
abscess  or  gangrenous  cavity  does  not  become  obliterated,  the  disease 
may  extend  through  the  visceral  layer  of  the  pleura  and  produce  a 
pneumothorax. 


572         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Spontaneous  pneumothorax  may  occur  without  gross  disease  of  the 
lungs  and  may  remain  simple  or  develop  an  effusion.  The  fluid  is 
serous  in  character  and  may  gradually  replace  the  air.  This  accident 
may  occur  as  the  result  of  rupture  of  an  emphysematous  bleb,  rupture 
of  interstitial  emphysema  or  a  tear  in  the  lung  as  the  result  of  traction  on 
an  adhesion  (Fig.  343). 

Symptoms. — The  onset  of  a  pneumothorax  is  sudden  in  about  three- 
fourths  of  the  cases.  0.  H.  P.  Pepper1  in  an  analysis  of  500  cases  from 
the  literature  in  which  the  onset  could  be  determined  accurately,  found 
that  in  77  per  cent,  the  onset  was  sudden  and  in  23  per  cent,  insidious. 


Fig.  343. — Pneumothorax.     Spontaneous  left-sided.     (Courtesy  of  Dr.  D.  R.  Bowen.) 

As  the  symptomatology  differs  according  to  whether  the  accident  is 
sudden  or  insidious  in  its  onset  the  two  types  will  be  considered  separately. 
When  the  onset  is  acute,  the  patient  is  suddenly  seized  with  an  agonizing 
pain  in  the  side  which  is  usually  felt  at  the  costal  margin.  The  pain  is 
often  referred  to  as  being  stabbing  or  tearing  in  character.  Coincidently 
with  the  onset  of  the  pain  there  is  great  difficulty  in  breathing.  Dyspnea 
is  perhaps  the  most  characteristic  feature  and  is  so  extreme  in  some  cases 
as  to  produce  a  feeling  of  impending  suffocation.  It  is  seen  in  its  most 
marked  form  in  advanced  cases  of  tuberculosis  where  in  addition  to  the 
collapsed  lung  there  is  apt  to  be  extensive  disease  on  the  opposite  side. 
1  Am.  Jour.  Med.  Sc,  October,  1911. 


DISEASES    OF   THE    PLEURA  573 

In  many  cases  there  is  every  evidence  of  severe  shock.  The  patient  is 
pale,  the  expression  anxious,  the  pulse  rapid  and  weak,  the  temperature 
falls,  the  extremities  are  cold  and  the  body  is  bathed  in  cold  sweat. 
This  picture,  however,  is  subject  to  many  variations;  some  of  the  symp- 
toms may  be  wanting  entirely  or  they  may  vary  greatly  as  to  their 
severity.  If  the  patient  survives,  the  accumulation  of  air  under  high 
tension  may  increase  the  difficulty  in  breathing  and  in  addition  there  is 
a  feeling  of  oppression  in  the  chest  or  distinct  pain. 

In  cases  with  an  insidious  onset  the  symptoms  which  characterize 
those  with  a  sudden  onset  may  be  lacking  entirely  or  they  are  so  trivial 
as  to  escape  notice.  Another  thing  which  contributes  toward  mask- 
ing a  pneumothorax  with  a  gradual  onset  is  the  fact  that  it  so  frequently 
occurs  in  patients  with  advanced  tuberculous  disease  of  the  lungs.  In 
patients  of  this  type  chest  pain,  dyspnea  and  tachycardia  are  nearly  al- 
ways present  and  may  vary  in  severity  from  time  to  time.  Under  the 
circumstances  a  pneumothorax  might  develop  without  attracting  notice. 
In  addition  an  exacerbation  of  one  or  all  of  these  symptoms  could  be 
attributed  readily  to  the  primary  disease.  The  number  of  times  that  a 
pneumothorax  is  discovered  accidently  either  by  physical  signs  or  an 
X-ray  examination,  or  is  first  revealed  at  the  autopsy  table  makes  it 
apparent  that  it  can  develop  either  without  symptoms  or  with  symptoms 
so  trivial  in  character  as  to  escape  notice. 

Physical  Signs. — Inspection. — If  the  patient  is  seen  shortly  after  the 
accident  he  is  apt  to  show  evidence  of  shock  and  extreme  dyspnea.  The 
posture  assumed  is  of  no  importance.  The  patient  usually  chooses  the 
position  which  is  most  comfortable;  this  may  be  lying  on  the  back,  on 
the  sound  side  or  the  affected  side.  If  the  dyspnea  is  marked,  the  patient 
may  assume  a  half-reclining  position  or  sit  leaning  forward. 

Displacement  of  the  heart  is  almost  constantly  noted  but  occasionally 
owing  to  the  lung  opposite  the  pneumothorax  being  firmly  adherent  to 
the  chest  wall  the  displacement  may  be  slight  or  not  occur  at  all.  Owing 
to  the  rapidity  of  the  respiratory  movements  and  the  weakness  of  the 
heart's  action  the  displacement  may  be  difficult  to  determine  by  means  of 
inspection. 

Of  the  utmost  importance  is  to  note  the  character  of  the  respiratory 
movements  of  the  two  sides.  If  the  pneumothorax  is  complete  it  will 
be  seen  that  on  the  affected  side  there  is  a  greatly  diminished  respiratory 
excursion  or  an  entire  absence  of  motion.  In  addition  the  interspaces 
are  partially  or  completely  obliterated. 

If  the  pneumothorax  has  existed  for  any  considerable  length  of  time 
the  unaffected  side  will  be  seen  to  expand  more  than  normally  as  the  result 
of  compensatory  emphysema  on  that  side.  In  long-standing  cases  of 
pyopneumothorax  the  affected  side  is  apt  to  become  retracted  as  in  cases 
of  empyema,  even  if  air  still  remains  in  the  pleural  cavity. 

Palpation. — Absent  or  greatly  diminished  tactile  fremitus  is  the  rule. 
In  some  instances,  however,  the  fremitus  is  retained.  Palpation  is  chiefly 
useful  in  confirming  the  presence  or  absence  of  expansion  and  is  also  an 
aid  in  determining  the  position  of  the  heart  and  displacement  of  the 
liver. 

Percussion. — The  character  of  the  percussion  note  over  a  pneumo- 
thorax is  variable.  As  a  rule,  it  is  tympanitic  in  quality  and  is  very 
similar  to  that  obtained  over  the  abdomen  when  the  intestines  are  dis- 


574         DISEASES    OF    THE   BROXCHI,    LTTNGS,    PLEURA,    AND    DIAPHRAGM 

tended  with  gas.  -  By  some  the  sound  is  referred  to  as  being  hyperreso- 
nant.     In  either  case  it  is  a  full  booming  note. 

Occasionally  the  air  within  the  pleural  cavity  may  be  under  such 
high  tension  as  to  give  rise  to  a  very  high-pitched  tympanitic  note 
scarcely  distinguishable  from  dulness.  In  still  other  instances  the  note 
may  sound  normal  in  character.  These  variations  may  be  due  in  part 
to  the  degree  of  tension  of  the  confined  air  and  in  part  to  variations  in  the 
sounding-board  properties  of  different  chest  walls. 

With  the  accumulation  of  fluid  the  tympanitic  or  hyperresonant  note 
merges  into  flatness  over  the  lower  part  of  the  chest.  The  existence  of 
fluid  can  sometimes  be  determined  by  the  presence  of  movable  dulness. 

In  estimating  the  value  of  a  tympanitic  note  on  the  left  side  it  should 
be  borne  in  mind  that,  at  times,  there  is  a  very  wide  area  of  stomach 
tympany  and  which  may  be  obtained  over  the  antero-lateral  aspect  of 
the  chest  as  high  as  the  fifth  rib.  This  error  can  be  avoided  by  noting 
the  position  of  the  heart  and  also  remembering  that  fluid  is  practically 
always  present.  In  the  latter  event  there  would  be  a  flat  note  below  the 
tympanitic  area. 

Auscultation. — The  breath  sounds  over  a  pneumothorax  are,  in  the 
majority  of  cases,  absent  or  very  distant.  When  present,  they  may  be 
of  any  character:  broncho-vesicular,  bronchial,  or  amphoric;  and  occa- 
sionally they  are  noted  as  being  vesicular  in  character.  Amphoric 
breathing  is  very  suggestive  of  pneumothorax  when  heard  over  the  middle 
and  lower  portions  of  the  chest.  It  may  be  loud  but  is  commonly  very 
distant  and  may  be  missed  unless  carefully  sought  for.  Occasionally 
the  heart  sounds  possess  a  metallic  quality. 

As  a  rule,  the  vocal  fremitus  is  absent  or  very  faint.  It  may,  however, 
be  normal  or  even  increased  in  intensity.  Pectoriloquy  is  noted  in  a  few 
cases. 

Rales  are  not  heard  over  the  pneumothorax.  Unless  the  lung  is 
completely  collapsed,  mixed  rales  will  be  heard  over  the  upper  part  of 
the  chest,  especially  in  the  tuberculous  cases. 

Vocal  resonance  may  be  absent,  diminished  in  intensity,  or  it  may 
have  an  amphoric  quality  (see  Fig.  57). 

Metallic  tinkle  is  a  sign  of  great  value,  when  present.  It  is  a  curious 
musical  echo  which  accompanies  the  breath  sounds  or  spoken  voice  or 
may  be  produced  by  coughing.  While  not  always  the  case  it  usually 
occurs  in  association  with  amphoric  breathing  and  amphoric  voice  sounds. 

Succussion  Splash. — This  is  the  oldest  and  the  most  certain  sign  of 
pneumothorax.  The  sound  is  produced  by  the  splashing  of  fluid  in  a 
resonating  cavity  containing  air.  To  elicit  the  succussion  splash,  the 
patient,  preferably  sitting  up,  is  sharply  shaken,  while  the  observer  has 
his  ear  or  stethoscope  applied  to  the  chest.  If  the  patient  is  not  too 
ill  he  may  be  made  to  shake  himself  so  as  to  produce  the  sound.  As 
in  the  case  of  other  sounds  produced  in  pneumothorax  the  succussion 
splash  has  a  metallic,  ringing  quality.  The  patient  himself  can  often 
hear  the  sound  or  feel  the  splashing  of  the  liquid. 

When  the  left  side  is  under  suspicion  one  must  bear  in  mind  that  the 
gurgling  sounds  over  the  stomach  have  a  metallic  quality  and  are  not  to 
be  confused  with  those  occurring  in  pneumothorax. 

The  Coin  Test. — Next  to  the  succussion  splash  this  is  the  most  certain 
single  symptom  encountered.     It  is  present  in  the  great  majority  of  cases 


DISEASES    OF   THE    PLEUKA  575 

and  when  heard  points  almost  conclusively  to  a  pneumothorax.  It  has 
been  noted  over  a  tuberculous  cavity  and  also  over  a  distended  stomach 
but  its  occurrence  under  such  circumstances  is  so  rare  that  it  may  be 
disregarded. 

If  there  is  every  reason  to  suspect  a  pneumothorax  and  the  coin  test  is 
not  at  once  evident  the  patient  should  be  examined  in  both  the  sitting 
and  recumbent  postures,  and,  in  addition,  the  coin  and  the  stethoscope 
should  be  placed  in  every  possible  relationship  to  each  other  before  a 
negative  finding  is  recorded.  The  coin  test  may  not  appear  for  the  first 
day  or  so  following  the  rupture. 

From  February  1,  1903,  to  February  1,  1910,  there  were  473  autopsies 
performed  in  the  Phipps  Institute  on  individuals  dying  of  pulmonary 
tuberculosis;  among  this  number  there  were  41  instances  of  pneumo- 
thorax, giving  a  percentage  of  8.6. 

These  cases  have  been  analysed  by  Stanton1  and  Cruice.2  The  fre- 
quency of  the  principal  physical  signs  noted  in  this  series  is  as  follows : 

Per  cent. 

Coin  test 90.61 

Expansion,  absent  or  restricted 89.00 

Hyperresonant  or  tympanitic  percussion  note 82 .  02 

Bulging  of  affected  side 77 .  04 

Breath  sounds: 

Distant 52.63 

Absent.. 18.42 

Amphoric 15 .  78 

Cavernous 7 .  59 

Broncho-vesicular .  . 5 .  20 

Metallic  tinkle 38. 88 

Succussion  splash 31 .  50 

Partial  Pneumothorax. — In  traumatic  cases  and  in  many  cases  of 
tuberculosis  the  pneumothorax  is  complete,  the  entire  lung  being  collapsed. 
In  a  very  considerable  proportion  of  cases,  however,  the  pneumothorax  is 
partial.  This  is  due  to  the  fact  that  the  lung  either  is  firmly  adherent  at 
some  point  to  the  chest  wall  or  to  the  diaphragm.  If,  therefore,  the  lung 
is  firmly  anchored  to  the  diaphragm  or  to  the  anterior  or  posterior  aspect 
of  the  chest  wall  it  cannot  completely  collapse  and  the  air  may  then 
occupy  only  a  part  of  the  pleural  cavity.  Figs.  344  and  345  show  how  a 
lung  adherent  to  the  lower  and  lateral  aspect  of  the  chest  wall  cannot 
completely  collapse.  In  such  cases  the  location  of  the  adhesion  will  de- 
termine whether  most  of  the  air  is  anterior  or  posterior. 

A  partial  pneumothorax,  if  sufficiently  large,  may  manifest  itself  by 
the  same  symptoms  as  the  complete  variety.  As  a  rule,  however,  symp- 
toms either  are  entirely  absent  or  so  trivial  as  to  pass  unnoticed.  If  the 
pneumothorax  is  relatively  large,  the  physical  signs  may  be  identical  with 
those  of  complete  pneumothorax  except  that  the  displacement  of  the 
heart  is  rarely  as  marked.  In  some  instances  the  physical  signs  of  a 
partial  pneumothorax  are  masked  by  the  pulmonary  disease.  This  has 
become  increasingly  evident  since  the  introduction  of  the  X-rays  in  ex- 
aminations of  the  chest.  In  other  instances  well-marked  physical  signs 
are  present   buti  are  incorrectly  interpreted.     This  was  true  in  the  case 

1  Fifth  Annual  Report  of  the  Phipps  Institute. 

2  Med.  Rec,  Sept.  23,  1911. 


576         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

shown  in  Fig.  345.  The  patient,  a  young  male,  had  been  complaining  of 
a  slight  cough,  malaise,  and  slight  loss  of  weight  for  several  weeks.  He  was 
suspected  of  having  early  tuberculosis.  The  examination  showed  re- 
striction of  motion  at  the  right  base.  The  percussion  note  over  the  base 
was  slightly  dull  except  for  an  area  below  the  angle  of  the  scapula  which 
was  tympanitic.  Over  the  dull  area  the  breath  and  voice  sounds  were 
distant;  over  the  tympanitic  area  there  was  distinct  whispering  pector- 
iloquy and  faint  amphoric  breath  sounds.  The  condition  seemed  to 
indicate  a  chronic  inflammatory  condition  of  the  left  base  with  dilatation 
of  the  bronchi  at  the  root  of  the  lung.  The  X-ray  examination  showed  a 
partial  pneumothorax  with  the  lung  adherent  at  a  point  laterally  and  at 


Fig.  344. — Left-sided  pneumothorax.  1,  Trachea.  2,  Esophagus.  3,  Superior  vena 
cava.     4,  Aorta.     5,  Vena  azygos. 

Section  at  the  level  of  the  second  intercostal  space.  The  left  lung  is  compressed  and 
adherent  to  the  costal  pleura.  The  right  lung  is  compensatorily  large.  The  superior  vena 
cava  is  compressed,  while  the  mediastinal  viscera  are  displaced  toward  the  right.  {After 
Pirogoff.) 

the  base.  Ten  days  later  the  foregoing  signs  had  disappeared.  The 
breath  sounds  were  perfectly  clear  except  at  the  extreme  base  where  the 
dulness  on  percussion  and  distant  breathing  pointed  to  a  small  effusion. 
A  second  X-ray  examination  confirmed  these  findings. 

In  the  majority  of  instances  a  partial  pneumothorax  is  located  at  some 
point  in  the  lower  part  of  the  chest.  Rarely  it  is  confined  to  the  upper 
portion.  In  the  absence  of  the  classical  signs  a  partial  pneumothorax  will 
usually  escape  detection  until  revealed  by  the  X-rays. 

Diagnosis. — Emphysema  is  usually  cited  as  one  of  the  conditions 
which  may  be  confused  with  pneumothorax. 

In  cases  of  spontaneous  pneumothorax  associated  with  emphysema  the 
percussion  note  over  the  emphysematous  lung  and  the  pneumothorax  may 
closely  resemble  each  other.  Hamman1  has  called  attention  to  the  value 
of  percussing  the  lower  lung  border.  Where  this  is  done  it  can  be  shown 
that  resonance  stops  on  the  affected  side  at  the  level  reached  by  the  lung 

1  Am.  Jour.  Med.  Sc,  February,  1916. 


DISEASES    OF    THE    PLEURA 


577 


on  the  sound  side  in  full  inspiration.  This  point  is  stationary,  showing 
no  variation  with  inspiration  and  expiration.  The  extension  of  pulmon- 
ary resonance  to  the  full  capacity  of  the  pleural  space  with  the  absence  of 
respiratory  variations  at  the  border  is  absolutely  characteristic  of 
pneumothorax  without  effusion. 

Pulmonary   Cavity  Due   to   Tuberculosis. — A  large  pulmonary  cavity 
may  simulate  a  pneumothorax  very  closely.     The  type  of  tuberculous 


Fig.  345. — Spontaneous  pneumothorax  on  right  side.  Adhesion  of  lung  to  lower  and 
lateral  aspect  of  chest  wall  has  presented  complete  collapse  of  lung.  (Roentgenogram  by 
Dr.  H.  K.  Pancoast.) 


case,  in  which  one  may  be  for  a  time  uncertain,  is  that  in  which  as  the 
result  of  a  chronic  ulcerative  process  nearly  the  entire  lung  has  become 
excavated.  In  extreme  cases  what  is  left  of  the  lung  is  no  more  than  a 
fibrous  shell  with  a  fringe  of  diseased  tissue  at  the  base  (see  Fig.  232). 

Over  the  remnants  of  such  a  lung  the  percussion  note  is  tympanitic, 
the  breath  sounds  may  be  amphoric  and  the  voice  sounds  have  a  metallic 
quality.  I  have  seen  cases  of  this  type  in  which  at  first  sight  the  presence 
of  a  pneumothorax  seemed  certain. 

37 


578  DISEASES    OF    THE    BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

An  error  can  be  avoided  if  the  following  facts  are  kept  in  mind :  The 
affected  side  is  retracted  instead  of  presenting  a  bulging  appearance;  the 
heart  instead  of  being  displaced  toward  the  sound  side  is  in  its  normal 
position  or  retracted  toward  the  diseased  side;  rales  can  often  be 
elicited  at  the  extreme  base  where  there  is  usually  some  remaining  lung 
tissue  and  finally  none  of  the  classic  signs  of  pneumothorax  (coin  test, 
metallic  tinkle,  succussion  splash)  can  be  elicited. 

Pleural  Effusion.- — Occasionally  a  tympanitic  percussion  note,  am- 
phoric breathing  and  a  metallic  quality  of  the  voice  sounds  can  be 
elicited  over  a  lung  compressed  as  the  result  of  an  effusion.  As  these 
signs  are  limited  to  the  extreme  upper  portion  of  the  chest  and  fluid  is 
demonstrable  immediately  below  one  should  not  be  deceived.  In 
pneumothorax  one  passes  from  below  upward  from  fluid  to  air  and 
thence  to  compressed  lung  tissue.  Still  the  simulation  may  be  very 
close.  I  recall  vividly  a  child  with  empyema  in  which  I  made  this  very 
mistake. 

A  pneumothorax  may  be  confused  with  diaphragmatic  hernia,  even- 
tration of  the  diaphragm  or  subphrenic  pyopneumothorax.  These 
conditions  are  considered  in  detail  in  the  chapter  on  "Diseases  of  the 
Diaphragm." 


CHAPTER  XXIV 

DISEASES   OF  THE  DIAPHRAGM 

In  spite  of  the  fact  that  a  knowledge  of  both  the  normal  and  the  patho- 
logical physiology  of  the  diaphragm  is  essential  to  a  proper  understand- 
ing of  many  thoracic  and  abdominal  affections,  references  to  this  structure 
are  scanty.  Most  of  the  standard  text-books  on  medicine  and  many  of 
those  dealing  with  diseases  of  the  chest,  either  omit  the  subject  entirely 
or  allude  to  it  only  in  a  cursory  fashion.  Although  rarely  the  primary 
seat  of  disease,  the  diaphragm  is  frequently  involved  in  nearly  all  pul- 
monary affections  and  in  many  of  the  inflammatory  conditions  involving 
the  upper  abdomen  The  neglect  of  the  diaphragm  was  emphasized  many 
years  ago  by  Walshe.1  "I  am  persuaded,"  he  wrote,  "much  of  their 
silence  depends  less  on  the  actual  immunity  from  disease  of  the  musculo- 
fibrous  septum,  than  upon  the  rarity  with  which  it  is  examined  post- 
mortem. Clinical  ignorance  is  the  necessary  result  of  this  neglect." 
Recently  the  role  played  by  the  diaphragm  in  inflammatory  affections 
of  the  lungs  and  pleura  and  the  upper  abdomen  has  received  more 
attention. 

ANATOMY 

The  diaphragm  is  a  great  musculo-fibrous  membrane,  composed  of 
muscle  and  fibrous  tissue  enclosed  within  two  serous  coats,  serving  as  a 
partition  between  the  cavities  of  the  thorax  and  abdomen.  It  presents 
a  double  dome  with  the  convexity  toward  the  thoracic  cavity. 

In  the  vaults  or  cavities  formed  by  the  arching  of  the  leaflets  are  con- 
tained on  the  right  side,  the  liver,  and  on  the  left  side  the  stomach  and 
spleen.  The  heart  rests  on  the  mid-die  portion.  Anteriorly  the  dia- 
phragm extends  as  high  as  the  fourth  interspace  on  the  right  side  and  to 
the  fifth  rib  on  the  left  side.  Posteriorly  the  right  arch  extends  to  the 
level  of  the  angle  of  the  scapula  (eighth  rib)  while  the  left  arch  lies  1 
inch  lower  (eighth  interspace).  The  central  tendon  reaches  the  level  of 
the  eighth  dorsal  spine.  Peripherally  the  diaphragm  arises  from  the 
posterior  surface  of  the  ensiform;  from  the  deep  surface  of  the  lower  six 
rib  cartilages  on  each  side  by  the  fleshy  bands  which  intermingle  with 
those  of  the  transversalis  abdominis;  and  from  the  lumbar  vertebrae,  the 
crura  and  the  arcuate  ligaments. 

The  main  nerve  supply  of  the  diaphragm  is  through  the  phrenics.  A 
narrow  portion  of  the  outer  rim  and  to  a  slight  extent  the  pleural  and 
peritoneal  coverings  also  receive  branches  from  the  intercostals  (sixth  to 
twelfth). 

The  diaphragm  is  exceedingly  rich  in  lymphatics  and  through  these 

vessels  the  communication  between  the  abdominal  and  thoracic  cavities 

is  free.     So  close  is  the  connection  that  infective  processes  may  pass 

readily  through  the  diaphragm  from  the  one  side  to  the  other.     A  knowl- 

1  "Diseases  of  the  Lungs,"  4th  cd.,  1871. 

579 


580  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

edge  of  this  fact  is  important  clinically,  as  it  will  often  make  clear  the 
pulmonary  symptoms  and  signs  which  not  infrequently  follow  abdominal 
lesions  or  operations,  particularly  those  in  the  right  upper  quadrant. 

PHYSIOLOGY 

Although  the  muscular  action  of  the  diaphragm  closely  resembles 
that  of  the  heart  in  its  rhythmic  repetition,  it  is  to  be  looked  upon  as 
being  both  a  voluntary  and  an  involuntary  muscle.  Under  ordinary 
conditions  it  performs  its  work  without  conscious  effort  on  the  part  of 
the  individual.  Its  action  can,  however,  be  voluntarily  arrested,  in- 
creased, or  checked  in  any  part  of  its  motion. 

The  normal  action  of  the  diaphragm  is  as  follows:  During  the  in- 
spiratory phase  the  two  leaflets  contract.  This  causes  the  two  dome-like 
projections  to  become  flattened  and  as  a  result  the  thoracic  cavity  is  en- 
larged downward  and  the  epigastrium  and  hypochondria  bulge  outward. 
At  the  same  time  the  distal,  arched  muscular  parts  become  flatter  and  are 
drawn  away  from  the  chest  wall  to  which  they  are  closely  applied  during 
relaxation  or  the  expiratory  phase.  The  middle  portion,  upon  which  the 
heart  rests,  takes  no  considerable  part  during  quiet  respiration;  but  during 
forced  breathing  it  is  depressed  also,  to  a  certain  extent. 

The  diaphragm  stands  in  the  same  relation  to  the  lower  surfaces  of  the 
lungs  as  the  chest  wall  does  to  other  portions  of  their  surface.  One  of  the 
chief  functions  of  the  diaphragm  is  to  keep  the  lower  parts  of  the  lungs 
fully  expanded.  If  this  fails  and  especially  if  the  lung  be  forced  upward 
by  the  unopposed  abdominal  muscles,  the  lower  part  of  the  lung  will 
collapse  just  as  failure  of  any  portion  of  the  chest  wall  to  expand  will  lead 
to  collapse  of  the  underlying  lung.  This  is  seen  clinically,  at  times,  as  a 
post-operative  condition.  As  a  result  of  paralysis  of  the  diaphragm 
massive  collapse  of  one  of  the  lower  lobes  occurs  (see  Atelectasis). 

The  muscular  action  of  the  diaphragm  differs  somewhat  from  that  of 
other  muscles  for  its  duration  is  from  four  to  eight  times  that  of  the  latter. 
It  is,  therefore,  to  be  regarded  as  a  tetanic  movement  of  short  duration 
(Landois) .  Of  the  ordinary  muscles  of  respiration  the  diaphragm  is  the 
most  important,  particularly  with  reference  to  the  part  it  plays  in  en- 
larging the  capacity  of  the  thorax.  In  this  regard  its  action  is  twofold: 
(1)  centrifugal  which  causes  an  elevation  of  the  ribs  thus  increasing  the 
transverse  and  antero-posterior  diameters  of  the  chest;  (2)  centripetal 
which  causes  a  drawing  downward  of  the  central  tendon  whereby  the 
vertical  diameter  is  increased.  In  the  recumbent  posture  (especially  in 
thin-chested  men)  with  the  light  falling  obliquely  on  the  side  of  the  thorax, 
the  contraction  of  the  diaphragm  can  often  be  seen  directly  in  the  form  of 
a  wave-like  movement  beginning  in  the  sixth  interspace  and  descending 
one  or  two  interspaces.  This  contraction  wave,  known  as  Litten's  sign, 
is  caused  by  the  peeling  off  of  the  diaphragm  from  the  sides  of  the  thorax. 
The  sign  is  of  some  diagnostic  value.  For  a  more  detailed  account  of 
Litten's  sign  see  page  31. 

Examined  by  means  of  the  fluoroscope,  the  two  sides  of  the  dia- 
phragm, under  normal  conditions,  are  seen  to  rise  and  fall  in  unison.  At  the 
end  of  expiration  the  dome  on  the  right  side  is  usually  higher  (about  one 
inch).  Not  only  is  the  fluoroscope  of  value  for  determining  the  motility 
and  contour  of  the  two  leaflets  but  in  addition  it  enables  us  to  inspect 


DISEASES    OF   THE    DIAPHRAGM 


581 


two  important  spaces.  One  lies  between  the  pericardium  and  the  dia- 
phragm and  is  called  the  phreno-pericardial  angle;  it  is  usually  more 
marked  on  the  right  side.  The  other  space  lies  between  the  outer  edge 
of  the  diaphragm  and  the  costal  surface.  This  is  known  as  the  phreno- 
costal  space  or  sulcus  (Fig.  346).  These  two  spaces  disappear  during 
expiration  but  during  inspiration  and  flattening  of  the  diaphragm  they 
reappear.  The  obliteration  of  these  spaces,  especially  the  phreno-costal, 
points  to  adhesions  or  immobility  of  the  diaphragm,  or  both.  The  action 
of  the  diaphragm  is  much  more  pronounced  in  men  than  in  women,  al- 
though occasionally,  as  in  the  case  of  trained  singers,  the  diaphragmatic 
action  in  women  is  similar  to  that  of  men.  Furthermore,  in  athletic 
men  the  excursions  of  the  diaphragm  are  much  greater  than  in  those  of 
sedentary  habits. 


Fig.  346. — Diaphragm.  Posterior  view.  A  A,  indicate  phrenocostal  spaces  which  are 
frequently  obliterated  by  adhesions.  Heart  is  seen  resting  on  the  diaphragm.  The 
phrenopericardial  angle  (more  marked  on  right  side)  is  also  frequently  obliterated  by 
adhesions. 

Rarely  marked  muscular  hypertrophy  may  occur  as  the  result  of  over- 
work caused  by  long  standing  abdominal  distention  (Fig.  347) .  Rolles- 
ton1  refers  to  a  patient  in  whom  marked  hypertrophy  of  the  diaphragm 
was  found  in  association  with  cirrhosis  of  the  liver  and  for  which  the 
Morison-Talma  operation  had  been  performed. 

The  nerve  supply  of  the  diaphragm  is  through  the  phrenic  nerves 
and  the  intercostals- (sixth  to  twelfth).  The  great  importance  of  the 
diaphragm  in  the  respiratory  process  can  be  realized  from  the  fact  that 
bilateral  action  of  the  phrenic  nerves  in  young  rabbits  is  followed  by 
death  (Landois).  A  knowledge  of  the  nerve  distribution  is  important  as 
pain,  the  result  of  inflammatory  or  other  conditions,  is  not  common  in 
the  diaphragm  itself.  The  pain  is  usually  referred  to  some  distant  point. 
These  painful  areas  are  often  associated  with  hyperasthesia  or -hyper- 
algesia of  the  skin  and  tenderness  on  pressure  (see  also  "Diaphragmatic 
Pleurisy,"  p.  535,  also  p.  43). 

1  "Diseases  of  the  Liver,"  1905. 


582         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

From  a  consideration  of  the  normal  and  pathological  physiology  of 
the  diaphragm  it  can  be  seen  that  this  muscle  is  a  most  important  factor 
in  the  respiratory  act.  Anything  which  interferes  with  its  work,  whether 
this  be  functional  or  organic  in  character,  is  apt  to  produce  a  more  or  less 
marked  disturbance.  The  disturbance  in  its  nervous  mechanism  has 
been  alluded  to.  Of  even  greater  importance  are  those  conditions  which 
produce  organic  changes  and  which  often  seriously  cripple  the  diaphragm. 


Fig.  347. — Section  showing  massive  ascites  surrounding  the  liver  and  intestines. 
The  diaphragm  is  pushed  upward,  compressing  the  lungs  and  turning  the  heart  into  a 
horizontal  position.      (Pirogoff.) 


FUNCTIONAL   DISTURBANCES    OF   THE    DIAPHRAGM 

Inhibition. — -A  very  common  deviation  from  the  normal  is  more  or 
less  inhibition  of  motion  of  one  or  both  of  the  leaflets.  Acute  inflamma- 
tion of  the  pleura  or  peritoneum  is  almost  constantly  attended  by  restric- 
tion in  the  movement  of  the  diaphragm.  In  such  cases  it  is  to  be  regarded 
as  protective  in  much  the  same  manner  as  inhibition  of  the  peristaltic 
movements  occurs  in  peritonitis.  In  unilateral  pulmonary  tuberculosis 
the  leaflet  on  the  affected  side  quite  constantly  shows  some  restriction  of 
motion  even  when  the  lesion  is  small  and  limited  to  the  apex.  This 
diminution  in  the  excursion  of  the  diaphragm  on  one  side  and  its  increased 
height  are  valuable  diagnostic  signs.  The  condition  can  be  determined 
beadily  by  the  fluoroscope  and  almost  equally  so  by  noting  the  diminished 
expiratory  excursion  and  the  higher  level  of  pulmonaiy  resonance  at  the 
case  on  the  affected  side  (see  p.  339,  also  Fig.  259). 


DISEASES    OF   THE    DIAPHRAGM  583 

Spasm  of  the  Diaphragm. — This  may  be  either  clonic  or  tonic  in 
character. 

Hiccough. — This  is  the  most  familiar  result  of  clonic  spasm.  The  con- 
dition is  caused  by  an  intermittent  and  sudden  spasm  of  the  diaphragm 
due  to  lesions  affecting  the  phrenic  nerves  at  their  origin  or  in  their 
course.  "  The  sound  is  produced  in  the  larynx  by  the  inrush  of  air  which 
follows  the  sudden  descent  of  the  diaphragm,  the  glottis  being,  so  to 
speak,  taken  unawares  in  a  condition  of  incomplete  dilatation"  (Fowler). 
It  may  recur  at  intervals  of  a  minute  or  so  or  the  intervals  may  be  so 
short  as  to  temporarily  interfere  with  breathing.  If  continued  for  an 
hour  or  so,  more  or  less  pain  is  apt  to  develop  along  the  line  of  attachment 
to  the  chest.  In  persistent  cases  extreme  exhaustion  may  take  place. 
In  the  majority  of  instances  hiccough  is  a  trifling  and  harmless  symptom 
which  lasts  for  a  few  minutes  and  then  ceases.  Occasionally,  however, 
it  becomes  persistent  and  uncontrollable  and  in  such  cases  is  to  be  re- 
garded with  the  greatest  apprehension.  It  has  been  known  to  continue 
for  months,  even  during  sleep.  As  one  of  the  terminal  events  in  fatal 
illnesses  hiccough  is  an  ominous  symptom  and  one  which  often  heralds 
approaching  dissolution. 

Hiccough  is  the  expression  of  reflex  irritation,  the  source  of  which 
may  be  above  or  below  the  diaphragm.  It  often  occurs  in  acute  inflam- 
matory conditions  of  the  abdominal  viscera,  in  the  severe  forms  of 
typhoid  fever  and  is  sometimes  observed  in  cases  of  pericarditis.  Its 
occurrence  in  such  cases  is  usually  indicative  of  danger.  Occasionally 
hiccough  is  an  annoying  post-operative  complication  particularly  after 
operations  in  the  upper  abdomen.  Hiccough  and  vomiting  often  occur 
as  the  result  of  gunshot  wounds  of  the  diaphragm. 

It  is  a  very  common  symptom  of  indigestion.  The  hiccough  which 
so  frequently  occurs  as  the  result  of  a  drinking  bout  is  of  this  variety. 
In  some  cases  the  source  of  irritation  is  in  the  central  nervous  system 
(apoplexy,  brain  tumor,  epilepsy).  It  may  occur  also  as  a  hysterical 
manifestation.  In  many  cases  it  is  apparently  idiopathic  as  no  demon- 
strable cause  can  be  found. 

Paroxysmal  sneezing  is  also  said  to  be  due  to  spasm  of  the  diaphragm 
although  the  contradictory  statement  is  made  that  the  induction  of 
sneezing  is  a  means  of  stopping  the  hiccough.  Laughing,  weeping  and 
coughing  spasms  are  of  much  the  same  nature  as  hiccough. 

Tonic  spasm  of  the  diaphragm  is  not  common.  It  occurs  in  tetanus, 
strychnine  poisoning  and  hydrophobia.  It  gives  rise  to  a  sense  of  con- 
striction in  the  chest,  intense  dyspnea  and  pain  along  the  insertion  of  the 
diaphragm. 

Paralysis  of  the  Diaphragm. — This  condition  may  be  caused  by  a 
central  or  a  peripheral  nerve  lesion.  Central  lesions  may  be  due  to 
caries  or  fracture  of  the  cervical  vertebrae,  tumor  of,  or  hemorrhage  into 
the  cord,  progressive  muscular  atrophy,  or  myelitis.  It  often  follows 
peripheral  lesions  in  which  the  phrenic  nerves  are  primarily  or  secondarily 
involved.  In  the  former  the  paralysis  may  follow  a  wound  in  the  neck 
which  injures  the  phrenic  nerve.  The  most  frequent  cause  of  paralysis 
of  the  diaphragm  is  diphtheria.  In  this  disease  the  diaphragmatic 
paralysis  almost  invariably  occurs  in  association  with  other  paralyses 
due  to  lesions  of  the  peripheral  nerves.  Any  condition  which  leads  to  a 
more  or  less  general  neuritis,  such  as  lead  poisoning,  anterior  poliomyelitis, 


584         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

or  Landry's  paralysis,  may  involve  the  phrenic  nerves.  Paresis  of  the 
diaphragm  sometimes  occurs  as  the  result  of  inflammation  of  the  serous 
covering  of  the  muscle. 

The  paralysis  may  be  unilateral  as  the  result  of  traumatic  injury  of 
the  phrenic  nerve  on  one  side,  or  bilateral  as  the  result  of  a  central  or 
peripheral  lesion.  The  latter  is  by  far  the  most  frequent.  When  the 
lesion  is  unilateral  the  symptoms  are  not  severe.  There  is  usually  some 
dyspnea.  The  severity  of  the  respiratory  symptoms  will  vary  consider- 
ably. The  base  of  the  lung  on  the  affected  side  may  become  congested 
or  there  may  be  a  localized  bronchitis  or  broncho-pneumonia.  The  con- 
dition should  be  suspected  in  case  of  a  wound  which  would  be  apt  to 
injure  the  phrenic  nerve.  Fluoroscopic  examination  will  show  the  arch 
on  the  affected  side  to  be  very  high. 

In  considering  the  physiology  of  the  diaphragm  it  was  pointed  out 
that  this  muscle  is  the  direct  expander  of  the  lower  lobes.  Paralysis  of 
the  muscle  may  cause,  therefore,  collapse  of  this  portion  of  the  lungs. 
Pasteur1  has  called  attention  to  the  occurrence  of  massive  collapse  of 
one  of  the  lower  lobes  as  a  post-operative  sequel.  The  collapse  may  be 
brought  about  in  some  cases  as  the  result  of  paralysis  of  one  of  the  leaflets 
of  the  diaphragm;  in  others  Pasteur  considers  it  to  be  due  to  reflex  in- 
hibition, caused  by  acute  inflammation  or  acute  pain  in  the  immediate 
neighborhood  of  the  diaphragm.  The  symptoms  and  signs  of  massive 
collapse  are  considered  under  "Atelectasis." 

Bilateral  paralysis  is  an  extremely  serious  condition,  and  may  lead 
rapidly  to  a  fatal  termination.  The  signs  and  symptoms,  as  given  by 
Fowler,  are  as  follows: 

1.  Reversal  of  the  respiratory  movements  of  the  epigastrium  and 
hypochondria.  These  regions  recede  during  inspiration  instead  of 
bulging. 

2.  Absence  of  downward  movement  of  the  abdominal  viscera  during 
inspiration. 

3.  Increased  movement  of  the  lower  ribs. 

4.  Dyspnea  on  exertion  or  excitement. 

5.  Alteration  in  the  character  of  the  voice  and  cough. 

6.  Loss  of  the  compressive  action  of  the  abdominal  muscles  upon  the 
contained  viscera  which  ordinarily  attends  such  acts  as  defecation,  and 
the  commencement  (but  not  the  continuance)  of  urination. 

7.  Feebleness  of  expiration  and  of  such  reflex  expiratory  actions  as 
cough,  sneezing,  expectorating,  are  direct  results  of  paralysis  of  the 
diaphragm;  as  the  presence  of  that  condition  presents  the  previous  in- 
spiration from  being  sufficiently  full  to  be  followed  by  a  forcible  expiratory 
act. 

8.  Diminution  of  the  total  capacity  of  the  thorax,  owing  to  the  in- 
creased arching  of  the  diaphragm. 

The  increased  horizontal  expansion  of  the  lower  thorax  and  reversal 
of  the  movement  of  the  epigastrium  and  hypochondria  are  typical  signs 
of  paralysis  of  the  diaphragm.  Fluoroscopic  examination  will  show  the 
absence  of  contraction  of  the  leaflets  and  the  abnormally  high  position 
of  the  arches.     They  may  extend  to  the  third  rib  or  even  higher. 

1  Annual  Oration,  Med.  Soc,  London,  May,  1911. 


DISEASES    OF   THE    DIAPHRAGM  585 

DIAPHRAGMATIC   HERNIA 

The  term  diaphragmatic  hernia  should  be  confined  to  those  instances 
in  which  the  abdominal  viscera  are  enclosed  in  a  sac  composed  of  all  or 
but  one  of  the  component  layers  of  the  diaphragm.  Stab  wounds  or 
other  traumatic  injuries  which  cause  a  rent  in  the  diaphragm  may  also 
lead  to  protrusion  of  parts  of  the  abdominal  viscera  into  the  thoracic 
cavity.  As  a  rule,  there  is  no  sac  but  in  some  cases  the  muscle  is  torn 
while  the  pleural  or  peritoneal  or  both  membranes  remain  intact.  This 
condition  should  be  termed  evisceration  and  not  hernia.  Likewise  the 
condition  known  as  eventration,  in  which  the  abdominal  viscera  extend 
high  into  the  thoracic  cavity  as  the  result  of  relaxation  of  the  diaphragm, 
should  not  be  confused  with  true  hernia.  Both  evisceration  and  even- 
tration will  be  considered  separately. 

Etiology. — Diaphragmatic  hernia  may  be  congenital  or  acquired. 
In  the  congenital  cases  the  defect  is  the  result  of  faulty  development. 
In  the  early  embryo  the  pleural  and  peritoneal  cavities  are  continuous. 
Later  they  become  separated  by  a  thin  membrane  which  extends  for- 
ward between  the  lungs  and  the  Wolffian  bodies.  This  membrane  is 
the  beginning  of  the  diaphragm,  the  development  of  which  may  be  ar- 
rested in  whole  or  in  part.  If  the  defect  is  extreme,  the  condition  will  be 
incompatible  with  life  and  is  met  with  in  still-born  children.  It  is  apt 
to  be  associated  with  other  congenital  defects.  If  the  defect  is  small, 
the  individual's  life  may  be  prolonged  indefinitely.  Rarely  an  individual 
with  an  extreme  defect  may  reach  adult  life.  Congenital  deficiency  of 
part  of  the  lateral  half  of  the  diaphragm  is  usually  placed  posteriorly 
and  on  the  left  side.  An  extraordinary  instance  of  this  was  recorded  by 
Henry  T.  Bowditch.1  A  male  adult  who  died  as  the  result  of  a  fractured 
spine  was  found  at  autopsy  to  have  most  of  the  left  side  of  the  diaphragm 
wanting;  so  that  the  stomach  and  greater  part  of  the  intestines  lay  in  the 
left  pleural  cavity.  The  lung  was  compressed  and  the  heart  displaced  to 
the  right  side.  The  condition  was  evidently  congenital.  In  addition 
to  absence  of  a  part  of  one  leaflet,  a  localized  bulging  or  pouching  due  to 
weakness  near  the  esophagus  or  xiphoid  cartilage  may  occur.  This  may 
be  the  result  of  a  congenital  defect  or  may  be  acquired.  In  the  latter 
instance  severe  straining  may  weaken  the  opening.  Rolleston2  is  of  the 
belief  that  in  not  a  few  cases,  what  is  thought  to  be  a  congenital  hernia 
is  in  reality  an  acquired  defect  due  to  a  forgotten  injury  received  years 
before.  The  condition  occurs  more  commonly  on  the  left  side.  Of 
74  cases  of  true  diaphragmatic  hernia,  Eppeniger3  found  21  on  the  right 
side  and  53  on  the  left. 

The  congenital  variety  is  not  apt  to  give  rise  to  symptoms.  The 
physical  signs  will  be  considered  under  "False  Hernia"  or  "Evisceration." 

EVISCERATION 

This  condition  is  often  referred  to  as  traumatic  hernia  or  hernia 
spuria. 

Etiology. — Evisceration  is  encountered  far  more  often  in  men  than  in 
women  for  the  reason  that  men  are  much  more  exposed  to  traumatic 

1  Buffalo  Med.  Jour.,  June  and  July,  1853. 

2  "Diseases  of  the  Liver,"  1905. 

3"Allg.  u.  Spez.  Path.  d.  Zwerchfells,"  Suppl.  Nortnogel's  Spez.  Path.  u. 
Therp.,  1911. 


586         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

injuries.  The  left  side  is  involved  in  over  90  per  cent,  of  the  cases. 
There  are  two  reasons  for  this:  First,  the  manner  in  which  the  injury 
commonly  occurs.  The  wound  is  usually  inflicted  by  a  right-handed 
person  striking  at  the  most  vital  and  most  accessible  part  of  his  oppon- 
ent, namely  the  left  side.  Second,  the  presence  of  the  liver  on  the  right 
side  acts  as  a  plug  if  an  opening  is  made.  Occasionally  a  part  of  the  liver 
may  pass  through  and  become  tightly  constricted  at  the  margin  of  the 
rent  like  a  strangulated  hernia.  Of  561  cases  of  hernia  spuria  or  evis- 
ceration, collected  by  Eppeniger  527  (95.6  per  cent.)  occurred  on  the 
left  side  and  34  (4.4  per  cent.)  on  the  right  side.  Green1  has  collected 
from  the  literature  123  cases  in  which  evisceration  has  followed  a  stab 
wound  of  the  diaphragm.  To  this  number  he  adds  six  personal  observa- 
tions. Protrusion  of  the  abdominal  viscera  into  the  thoracic  cavity 
occurs  in  a  little  over  50  per  cent,  of  stab  wounds. 

In  addition  to  stab  wounds  evisceration  may  follow  injury  of  the 
diaphragm  as  the  result  of  gunshot  wounds  (a  not  infrequent  occurrence 
in  the  present  war),  severe  straining,  crushing  accidents,  or  a  blow  on  the 
chest.  A  strain,  a  blow  or  a  crushing  accident  may  simply  tear  the 
muscle,  leaving  the  serous  coverings  intact.  This  group  is  the  most 
difficult  of  recognition  as  there  is  no  visible  wound  and  the  symptoms 
are  often  misleading. 

Symptoms. — The  initial  symptoms  are  those  of  shock  from  which  the 
patient  may  die  immediately.  Pain  is  rarely  severe  but  there  is  usually 
a  feeling  of  constriction  in  the  chest.  Dyspnea  is  usually  severe  and 
may  follow  the  injury  almost  immediately.  Not  infrequently,  however, 
it  is  a  late  manifestation.  In  left-sided  cases  vomiting  is  one  of  the  most 
constant  symptoms.  In  the  case  of  gunshot  wounds  Keogh  Murphy2 
states  that  the  two  most  important  symptoms  are  vomiting  and  hic- 
cough and  that  other  signs  of  perforation  of  the  diaphragm  are  usually 
absent.  Makins3  states  that  perforation  of- the  diaphragm  with  a  small- 
bore bullet  is  of  no  great  significance  unless  the  course  taken  by  the 
bullet  is  such  that  a  more  or  less  extensive  slit  results.  In  such  cases 
the  respirations  are  shallow,  often  accompanied  by  a  groan  or  the 
slightest  degree  of  hiccough  on  inspiration  and  a  considerable  increase 
in  respiratory  frequency.  Pleurisy  or  peritonitis  or  both  are  apt  to 
develop  after  a  wound.  If  the  patient  survives  he  gradually  recovers 
strength  and  may  suffer  but  little  inconvenience.  As  a  rule,  however, 
an  irritating  cough  develops,  dyspnea  becomes  marked  on  exertion,  and 
there  is  pain  in  the  chest.  In  addition  there  is  more  or  less  marked  dis- 
turbance of  the  digestive  process  consisting  of  collicky  pains,  constipa- 
tion and  vomiting.     Emaciation  often  occurs. 

Physical  Signs. — With  few  exceptions  the  physical  signs  are  limited 
to   the  left  side. 

Inspection. — If  a  wound  has  been  received  its  location  is  of  great  im- 
portance. The  presence  of  a  wound  associated  with  diaphragmatic 
symptoms  (vomiting,  hiccough,  dyspnea,  etc.)  may  be  sufficient  to  es- 
tablish the  diagnosis.  In  the  case  of  stab  wounds,  the  protrusion  of  a 
piece  of  omentum  through  the  external  wound  is  very  common.  Flat- 
tening of  the  abdomen  and  distention  of  the  lower  part  of  the  chest, 

1  Jour.  Am.  Med.  Assoc,  July  15,  1916. 

2  "Wounds  of  the  Thorax  in  War,"  1915. 

3  "Surgical  Experiences  in  South  Africa,  1S99-1900." 


DISEASES    OF   THE    DIAPHRAGM  587 

proportional  to  the  quantity  of  viscera  carried  into  the  thoracic  viscera, 
are  frequently  present.  If  the  rent  is  large,  the  heart  is  displaced  to  the 
right  or  upward  and,  owing  to  compression  of  the  lung,  expansion  on  the 
left  side  is  restricted. 

Palpation. — This  may  show  an  absence  of  tactile  fremitus  at  the  left 
base  and  the  displacement  of  the  heart  to  the  right  or  upward. 

Percussion. — As  a  rule  the  percussion  note  is  tympanitic  at  the  left 
base.  It  may,  however,  be  toneless  owing  to  the  displacement  of  the 
spleen  through  the  opening  or  to  the  presence  of  a  hemothorax.     Rarely 


Fig.  348. — Traumatic  hernia  of  diaphragm.  Dark  shadow  below  is  caused  by  bis- 
muth. Upper  line  of  stomach  can  be  seen  through  the  lung  shadow.  (Courtesy  of  Dr.  H. 
K.  Pancoast.) 

the  intestines  may  extend  over  to  the  right  side  in  which  case  there  is 
pulmonary  resonance  above  the  tympany  and  liver  dulness  below. 

Auscultation. — Breath  sounds  will  be  absent  at  the  base  of  the  left 
lung  and  audible  along  the  spine  and  upper  portion  of  the  chest.  Gurg- 
ling sounds  due  to  the  movement  of  flatus  or  fluid  in  the  displaced  hollow 
viscera  may  be  heard. 

X-ray  Examination. — Examined  by  means  of  the  fluoroscope  or 
radiograph  the  contour  of  the  arch  on  the  affected  side  is  seen  to  be 
abnormal.  Becker  gives  the  following  description:  The  line  is  irregular, 
being  fairly  clear  at  some  points  and  blurred  in  others.  There  is  usually 
a  reversal  of  the  normal  respiratory  movement.  If  bismuth  is  given, 
the  upper  line  of  the  dome  becomes  very  irregular  from  the  new  shadows; 


588         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

if  the  stomach  is  distended  with  CO2,  the  upper  line  extends  very  high 
and  lung  shadows  mav  be  seen  through  the  distended  stomach  (Figs. 
348  and  349). 

Diagnosis. — The  condition  is  most  apt  to  be  confused  with  pneumo- 
thorax, especially  in  those  cases  in  which  there  has  been  no  obvious 
wound.  From  the  latter  evisceration  may  be  distinguished  by  the  ab- 
dominal flattening,  restriction  of  motion  of  left  chest,  absence  of  bulging 
of  the  intercostal  spaces,  absence  of  breath  sounds  and  the  presence  of 
gurgling  sounds  peculiar  to  the  stomach  and  intestines.     Examination 


Fig.  349. — Same  as  Fig.  34S.     Showing  bismuth  in  the  stomach. 

with  the  X-rays  will  readily  distinguish  the  two  conditions.  Eviscera- 
tion is  also  to  be  distinguished  from  eventration  which  is  next  to  be 
considered. 


EVENTRATION  OF  THE  DIAPHRAGM 

Eventration  is  a  relatively  rare  condition.  It  is  characterized  by  a 
general  expansion  of  one-half  of  the  diaphragm  allowing  the  abdominal 
viscera  to  be  displaced  upward  into  the  thoracic  cavity.  It  differs 
from  hernia  and  evisceration  in  that  the  contour  of  the  affected  dome  is 
not  irregular.  There  is  neither  a  bulging  nor  a  localized  opening  (Fig. 
350).  Various  names  have  been  applied  to  the  condition,  the  terms  em- 
ployed being  more  or  less  descriptive  of  what  is  presumed  to  be  the 
anatomical  factor.  Thus  it  has  been  referred  to  as  insufficiency,  relaxa- 
tion, dilatation,    high  position  or  elevation  of  the  diaphragm. 


DISEASES    OF    THE    DIAPHRAGM 


589 


Etiology. — There  are  two  hypotheses  as  to  the  cause  of  the  abnormally 
high  position  of  the  diaphragm. 

1.  It  is  believed  by  some  to  be  due  to  increased  abdominal  tension  long 
continued.     There  is  little   to   support   this   view.     An   overwhelming 


Fig.  350. — Eventration  of  the  diaphragm.    (Courtesy  of  Dr.  D.  R.  Bowen.) 


majority  of  the  cases  have  occurred  in  males.  Women  who  have  passed 
through  a  number  of  pregnancies  are  not  predisposed  to  the  condition  in 
spite  of  the  abdominal  pressure.  Furthermore,  it  has  been  encountered 
in  infants  and  young  children. 


590         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

2.  The  weight  of  opinion  is  in  favor  of  a  congenital  origin.  The  points 
in  favor  of  this  are  that  it  does  occur  in  infants;  the  lung  on  the  affected 
side  is  not  compressed;  and  finally  there  is  no  history  of  traumatism 
or  acute  infection  which  might  lead  to  weakness  or  relaxation  of  the 
diaphragm. 

It  is  a  rare  condition.  In  a  study  of  652  cases  of  hernia,  both  true  and 
false,  and  eventration,  Eppeniger  found  but  17  examples  of  the  latter. 
Recently  Bayne-Jones1  reported  45  cases  from  the  literature.  His  paper 
contains  all  that  is  known  on  the  subject.  Males  are  affected  in  the 
great  majority  of  cases.  Of  the  45  cases  so  far  recorded  all  but  3  have 
occurred  on  the  left  side. 

Symptoms. — As  the  condition  is  congenital  and  the  development  of 
the  thoracic  and  abdominal  organs  compensates  for  the  abnormality,  there 
are  no  symptoms.  It  is  usually  an  accidental  discovery  which  may  be 
made  in  a  routine  physical  or  X-ray  examination  or  at  the  autopsy  table. 

Physical  Signs. — Of  the  three  cases  occurring  on  the  right  side  the  one 
reported  by  Bayne-Jones  is  the  only  one  recognized  during  life.  In  this 
case  there  was  absence  of  Litten's  shadow  and  dulness  and  absent  breath 
sounds  between  the  third  and  fifth  ribs.  Above  the  dull  area  there  was 
pulmonary  resonance  and  below  it  tympany.  Inflation  of  the  colon  dis- 
placed the  dull  area  upward  and  increased  the  area  of  tympany. 

In  the  left-sided  cases  there  is  an  abnormally  large  area  of  tympany 
both  front  and  back.  Over  this  area  the  breath  sounds  are  absent  and 
there  may  be  gurgling  sounds  due  to  the  movement  of  fluid  in  the  stomach 
or  flatus.  The  lung  is  not  compressed  but  the  heart  may  be  displaced  to 
the  right  or  upward. 

The  radiographic  picture  is  as  follows:  The  contour  of  the  dome  is 
that  of  a  smooth,  sharply  defined,  bow-shaped  shadow  with  a  bright  area 
below  and  lung  shadows  above.  If  bismuth  be  given  the  stomach  and 
intestines  form  new  shadows.  In  a  case  seen  by  Norris  (shown  in  Fig. 
350)  at  the  Pennsylvania  Hospital  the  percussion  note  over  the  left  chest 
both  anteriorly  and  posteriorly,  especially  from  the  sixth  rib  downward, 
was  very  tympanitic.  On  auscultation  the  breath  sounds  were  bron- 
cho-vesicular and  in  addition  inconstant,  muscial,  splashing  and  gurgling 
sounds  were  heard  such  as  usually-  occur  in  association  with  hyperperis- 
talsis.  The  patient  came  to  the  hospital  because  of  abdominal  pain. 
He  was  later  operated  on  for  a  gastric  ulcer  which  was  found  to  be 
present.  Exploration  on  the  left  side  revealed  a  very  high  but  apparently 
normal  diaphragm.  A  very  long  and  large  stomach,  the  left  flexure  of 
the  colon  and  a  portion  of  the  small  intestines  occupied  the  space  created 
by  the  high  diaphragm. 

Diagnosis. — The  condition  may  be  confused  with  pneumothorax,  a 
large  basal  cavity,  a  subphrenic  abscess  producing  gas,  paralysis  of  the 
diaphragm  and  hernia. 

The  essential  feature  of  eventration  is  that  it  is  not  proceeded  by 
symptoms,  either  acute  or  chronic,  while  all  of  the  conditions  just  men- 
tioned are,  with  the  possible  exception  of  a  latent  pneumothorax.  Even 
in  cases  of  latent  pneumothorax  the  history  is  apt  to  throw  some  light  on 
the  condition  as  it  is  so  commonly  due  to  tuberculosis. 

A  large  cavity  would  be  associated  with  marked  respiratory  symptoms 
and  other  signs  of  thoracic  damage.  In  subphrenic  gas  abscess  there 
1  Arch.  Int.  Med.,  February,  1916. 


DISEASES    OF    THE    DIAPHRAGM  591 

would  be  pain,  fever  and  other  evidences  of  sepsis.  Paralysis  of  the 
diaphragm  is  usually  bilateral.  If  unilateral,  it  is  usually  due  to  a 
traumatic  injury  of  the  phrenic  nerve  or  to  paresis  following  some  acute 
thoracic  affection,  such  as  empyema.  Hernia  and  evisceration  both 
produce  marked  changes  in  the  thoracic  viscera  (displacement  of  the 
heart  and  compression  of  the  lung)  and  in  the  case  of  the  latter  there  is  a 
history  of  trauma. 

Fluoroscopic  and  radiographic  examinations  are  the  most  certain 
means  of  recognizing  the  condition. 

DIAPHRAGM  ATIS 

Inflammation  of  the  serous  covering  of  the  diaphragm  is  relatively 
common.  The  pleural  surface  is  most  frequently  involved  and  in  such 
instances  the  clinical  picture  is  fairly  definite  (see  "Diaphragmatic 
Pleurisy"). 

Primary  Diaphragmatis. — The  muscle  itself  is  rarely  the  primary  seat 
of  inflammatory  changes.  The  best  known  example  of  primary  inflam- 
mation of  the  diaphragmatic  muscle  is  seen  in  trichiniasis.  The  trichina 
spiralis  very  frequently  invades  the  diaphragm  and  in  some  instances  sets 
up  a  serious  myositis.  Steiner1  states  that  the  diaphragm  may  become  so 
extensively  involved  by  the  parasite  as  to  produce  paralysis  of  the  muscle 
and  death.  In  this  connection  it  might  be  mentioned  that  in  addition  to 
changes  in  the  diaphragm,  respiratory  symptoms  are  often  due  to  invasion 
of  the  pulmonary  tissue  by  the  trichinse.  The  embryos  may  be  demon- 
strated in  the  lungs  and  in  such  cases  lobar  or  broncho-pneumonia, 
hypostatic  congestion  or  hemorrhagic  areas  are  frequently  present. 
Minot  and  Rackemann2  in  an  analysis  of  the  symptoms  in  102  cases  of 
trichiniasis  found  that  one-half  had  respiratory  symptoms  or  signs  or 
both.  In  a  few  instances  the  pulmonary  symptoms  and  signs  were  so 
prominent  as  to  lead  to  a  serious  consideration  or  actual  diagnosis  of  a 
purely  pulmonary  condition. 

In  the  terminal  stages  of  scurvy  a  most  intense  form  of  dyspnea  and  a 
feeling  of  constriction  at  the  base  of  the  chest  sometimes  occurs  independ- 
ent of  any  lesion  in  the  lungs.  In  these  cases  there  is  often  a  brawny 
induration  of  the  diaphragm  or  rupture  of  the  muscle  fibers  and  hemor- 
rhage, identical  in  nature  with  that  occurring  in  the  voluntary  muscles. 

A  routine  examination  of  the  diaphragm  both  grossly  and  micro- 
scopically would  doubtless  show  that  the  various  structures  of  the  dia- 
phragm are  more  frequently  the  seat  of  pathological  changes  than  is  at 
present  believed.  Walshe3  states  that  he  not  infrequently  noted  a  red, 
patchy,  and  ecchymotic  discoloration  of  the  muscle  fibers;  softening  of  the 
muscle  or  central  tendon;  and  infiltration  (serous,  exudative  or  purulent) 
of  the  connective  tissue. 

Secondary  Diaphragmatis. — This  is  a  common  condition  and  occurs 
far  more  frequently  than  is  generally  taught  in  the  text-books. 

Etiology. — The  most  frequent  cause  is  an  inflammatory  condition 
involving  either  the  thoracic  or  abdominal  viscera.  The  former  is  by  far 
the  most  important.     Although  croupous  or  broncho-pneumonia  may 

1  Boston  Med.  &  Surg.  Jour.,  1908,  cvi,  721. 

2  Am.  Jour.  Med.  Sc.,  October,  1915. 

3  Diseases  of  the  Lungs,  4th  ed.,  1871. 


592         DISEASES    OF   THE   BBOXCHI,    LUNGS,    PLEURA,    AXD    DIAPHRAGM 

produce  inflammatory  changes  in  the  diaphragm  they  are,  as  a  rule,  mild 
and  leave  no  permanent  changes.  The  most  serious  secondary  changes  in 
the  diaphragm  follow  inflammatory  conditions  of  the  pleura.  The 
primary  trouble  in  the  pleura  may  be  a  simple,  dry  pleurisy,  a  serofi- 
brinous pleurisy  or  empyema.  Effusions,  especially  if  purulent,  are 
especially  apt  to  damage  the  diaphragm.  Pneumoconiosis  is  a  common 
cause  of  immobility.  The  frequency  with  which  the  pleura  becomes  the 
seat  of  inflammatory  changes  in  tuberculosis  makes  the  latter  disease  a 
most  important  factor  in  changes  involving  the  diaphragm. 

Aside  from  noting  the  motility  and  position  of  the  diaphragm,  little 
has  been  done  toward  ascertaining  the  changes  which  occur  in  the  muscle 
in  tuberculous  cases.  White1  determined  the  height  of  the  diaphragm  at 
autopsy  in  187  cases  of  tuberculosis.  In  44  instances  (27  right  side,  17 
left  side)  the  diaphragm  extended  as  high  as  the  fourth  rib  to  third  inter- 
space. In  34  (20  right  side,  14  left  side)  it  was  abnormally  low,  ranging 
from  the  sixth  rib  to  the  eighth  interspace.  Pryor2  has  reported  a  study 
of  the  diaphragm  in  84  patients  who  had  had  an  effusion.  Of  these  cases 
47  were  instances  of  empyema;  16  of  pleural  effusion;  and  21  of  effusion 
associated  with  pulmonary  tuberculosis.  In  the  entire  series  the  move- 
ment of  the  diaphragm  on  the  affected  side  was  normal  in  14,  more  or  less 
restricted  in  16,  and  entirely  lost  in  54.  Thus  it  is  seen  that  but  one  out 
of  every  fourteen  escaped  some  damage  to  the  diaphragm.  Empyema  is 
by  far  the  most  serious  condition  so  far  as  the  diaphragm  is  concerned. 
As  a  rule  but  one  side  of  the  diaphragm  is  involved,  but  occasionally  the 
condition  may  be  bilateral. 

Morbid  Anatomy. — It  is  after  all  not  surprising  that  the  diaphragm 
should  be  subject  to  inflammatory  changes  when  we  recall  its  rich 
lymphatic  supply.  Through  these  channels  bacteria  may  be  carried 
upward  from  some  point  of  infection  in  the  abdomen  or,  what  more 
commonly  happens,  the  infection  may  occur  from  the  lungs  or  pleura. 
It  is  almost  inevitable  that  a  structure  bathed  in  the  pus  of  an  empyema 
will  undergo  inflammatory  changes.  In  the  early  stage  of  diaphragmatitis 
the  muscle  feels  like  a  sodden,  doughy  mass  of  infiltrated  tissue.  In 
addition  it  is  stiff,  unyielding  and  more  or  less  thickened.  Next,  the 
muscle  loses  its  elasticity  and  becomes  quite  rigid.  Finally,  it  becomes 
atrophied  and  as  the  result  of  fibroid  change,  hard  and  immovable.  As  a 
rule  the  affected  leaflet  becomes  fixed  in  the  low  or  below  the  middle 
position.  An  additional  factor  in  producing  injury  of  the  diaphragm  in 
cases  of  effusion  is  the  weight  of  fluid  which  has  often  been  present  for 
months.  In  the  case  of  a  large  and  unrecognized  empyema  it  is  no 
unusual  thing  at  the  autopsy  table  to  find  that  the  leaflet  on  the  affected 
side  is  turned  inside  out,  the  convexny  being  toward  the  abdomen  (see 
Figs.  326  and  327) .  This  is  due,  in  part,  to  loss  of  function  and  elasticity, 
the  result  of  inflammatorv  changes,  and,  in  part,  to  the  weight  of  the 
fluid. 

Associated  with  changes  in  the  structure  of  the  diaphragm  are  adhe- 
sions. In  some  instances,  as  in  the  case  of  dry  pleurisy,  the  adhesions 
probably  occur  first  and  the  chronic  inflammatory  changes  in  the  muscle 
occur  secondarily.  In  the  case  of  effusions  it  is  probable  that  the  loss  of 
function  is  primarily  due  to  changes  in  the  diaphragm  itself  and  that 

1  Fifth  Annual  Report,  Phipps  Institute,  1908. 

2  International  Clinics,  vol.  ii,  Twenty-sixth  Series,  1916. 


DISEASES    OF    THE    DIAPHRAGM 


593 


later  adhesions  form  which  serve  to  anchor  the  diaphragm  in  its  abnormal 
position,  so  that  even  if  the  muscle  does  recover,  the  adhesions  prevent  the 
leaflet  from  asssuming  its  normal  position  and  function.  The  portions 
most  likely  to  be  affected  are  the  spaces  between  the  pericardium  and  the 
diaphragm  and  the  phrenocostal  sulcus.  The  latter  forming  the  most 
dependent  portion  of  the  pleural  space,  may  retain  a  small  amount  of 
fluid  and  sediment  which  tend  to  favor  adhesions  even  when  the  aspira- 
tion has  been  most  complete  (Figs.  351  and  352) .  As  a  result  of  adhesions 
at  these  points,  the  affected  leaflet  becomes  more  or  less  fixed  and  loses 


Fig.   351. — Obliteration  of  complementary  pleural  space  and  adhesion  of  diaphragm 
to  chest  wall  on  right  side,  following   a  pleural  effusion.     (Roentgenogram  by  Dr.  H.  K 
Pancoast.) 


its  normal  contour.  It  may  be  motionless,  move  but  slighty  or  one  por- 
tion may  show  motion  while  another  remains  fixed.  The  heart  is  apt  to 
be  drawn  toward  the  middle  line  and  the  lower  lobe  of  the  lung  may  be- 
come more  or  less  atelectatic  as  the  aspirating  power  of  the  lung  upon  the 
diaphragm  diminishes  or  ceases. 

Symptoms. — The  chief  symptoms  of  immobility  of  the  diaphragm 
following  inflammatory  changes  are  dyspnea  and  soreness  or  a  sense  of 
(hugging  in  the  lower  part  of  the  chest  which  may  persist  for  a  long  time 
after  paracentesis.     Interference  with  the  heart's  action  due  to  adhesions 

38 


594         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

may  occur  also.  The  dyspnea  as  a  rule  occurs  only  on  exertion.  In 
tuberculous  cases  dyspnea  at  times  is  very  marked  and  is  out  of  propor- 
tion to  the  amount  of  pulmonary  damage.  It  is  quite  probable  that  a 
more  careful  study  of  these  cases  will  show  that  immobility  of  the  dia- 
phragm is  the  underlying  cause  of  the  dyspnea.  If  both  leaflets  are 
immobile  the  dyspnea  will  be  marked.     Pry  or1  has  reported  a  case  in 


Fig.  352. — Left  leaflet  of  the  diaphragm  flattened  and  adherent  to  chest  wall.  Phreno- 
costal  space  is  obliterated,  following  empyema.  {Roentgenogram  by  Dr.  H.  K.  Pan- 
coast.) 

which  both  sides  of  the  diaphragm  were  immovable  and  fixed  in  their 
lowest  position.  In  a  patient  seen  at  the  Phipps  Institute  in  whom  both 
lower  lobes  were  the  seat  of  a  chronic  blastomycotic  infection  there  were 
frequent  paroxysms  of  dyspnea  which  were  characterized  by  rapid  and 
shallow  breathing  and  cyanosis;  fluoroscopic  examination  showed  very 

1  hoc.  cit. 


DISEASES    OF    THE    DIAPHRAGM 


595 


little  diaphragmatic  movement  on  either  side  and  on  the  left  side  the 
phrenocostal  sulcus  was  obliterated  by  adhesions  (Fig.  353). 

Physical  Signs. — Immobility  of  the  diaphragm  is  seen  in  its  most 
characteristic  form  following  a  pleural  effusion.  If  the  effusion  has 
been  present  but  a  few  days  the  lung  quickly  expands  and  in  the  course 
of  a  few  clays  little  change  is  to  be  noted.     In  these  cases  it  is  probable 


Fig.  353. — The  dense  shadows  at  both  bases  are  due  to  a  chronic  blastomycosis.  Both 
leaflets  are  high  and  on  fluoroscopic  examination  show  scarcely  any  motion.  Patient  sub- 
ject to  frequent  attacks  of  dyspnea.     {Roentgenogram,  by  Dr.  H.  K.  Pancoast.) 

that  the  diaphragm  has  escaped  with  little  or  no  injury.  On  the  other 
hand,  if  the  effusion  has  been  present  for  some  time  the  most  marked 
physical  signs  persist  at  the  base  of  the  affected  chest  in  spite  of  the  re- 
moval of  a  large  amount  of  fluid.  The  usually  accepted  teaching  has  been 
that  the  lung  has  failed  to  expand.  While  this  is  in  a  measure  true  the 
major  portion  of  the  difficulty  is  to  be  ascribed  to  crippling  of  the  functions 
of  the  diaphragm.  This  may  be  transitory  in  character  or  it  may  be 
permanent. 


596         DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Absence  of  Litten's  sign,  restriction  of  motion,  dulness  on  percussion 
and  distant  or  suppressed  breath  sounds  are  the  most  prominent  of  the 
physical  signs. 

The  most  certain  method  of  determining  the  condition  of  the  dia- 
phragm and  its  functional  capacity  is  direct  inspection  by  means  of  the 
fruoroscope  or  a  radiograph. 

In  pulmonary  tuberculosis,  even  when  the  disease  is  confined  to  a  limited 
area  in  one  apex,  the  diaphragm  on  the  affected  side  often  shows  a  dimin- 
ished inspiratory  descent  when  examined  with  the  fluoroscope.  This 
is  known  as  Williams'  early  diaphragmatic  sign.  Walsham  and  Over- 
end1  offer  the  following  explanation  of  this  phenomenon:  (1)  Pleuritic 
adhesion,  at  the  apex,  or  perhaps  at  the  base;  (2)  impairment  of  retractile 
pulmonary  elasticity;  (3)  reflex  inhibition  of  muscular  action  from 
mechanical  irritation  of  the  terminal  fibers  of  the  vagus,  which  might 
affect  the  corresponding  half  of  the  diaphragm,  or  the  bronchial  muscula- 
ture, or  possibly  both;  (4)  the  phrenic  nerve  fibers  might  be  directly  in- 
volved at  the  apex.  Unilateral  diminution  in  the  inspiratory  descent  of 
the  diaphragm  can  be  determined  also  by  percussion.  This  is  done  by 
marking  out  the  base  of  the  lung,  front  and  back,  first  while  at  rest,  and 
then  after  a  deep  inspiration.  Even  in  very  early  cases  of  tuberculosis, 
while  there  is  still  only  a  small  involvement  at  the  apex,  the  effect  upon 
the  function  of  the  lung  of  such  a  focus  is  such  that  there  will  be  a  distinct 
limitation  of  motion  on  the  affected  side  (see  p.  339). 

SUBDIAPHRAGMATIC  ABSCESS 
(Subphrenic  Abscess,  Subphrenic  Peritonitis) 

Although  entirely  extrathoracic,  at  least  in  the  beginning,  a  localized 
collection  of  pus  in  contact  with  the  under  surface  of  the  diaphragm  must 
nearly  always  be  differentiated  from  analogous  conditions  above  the 
diaphragm  or  within  the  thoracic  cavity.  Subdiaphragmatic  abscess  is 
of  great  interest  to  the  student  of  thoracic  affections  not  only  because  of 
the  problem  involved  in  determining  the  location  of  the  pus  but  also 
because  of  the  frequency  with  which  the  thoracic  contents  are  secondarily 
implicated.  Thus  of  173  cases  collected  by  Lang2  thoracic  complications 
were  present  in  140  or  82  per  cent.;  pleurisy,  serous  or  serofibrinous  in 
41;  empyema  in  16;  pericarditis  in  16;  adhesions  between  the  lung  and 
diaphragm  and  ulceration  through  the  diaphragm  in  7;  perforation  into 
the  lung  occurred  in  34,  into  the  pleural  space  in  23  and  into  the  peri- 
cardium in  3  cases.  Picque3  emphasizes  the  fact  that  although  anatom- 
ically the  abscess  is  below  the  diaphragm,  it  is  actually  within  the  thorax. 
In  most  cases  there  will  be  little  difference  in  the  physical  signs  between 
a  localized  collection  of  pus  above  the  diaphragm  pushing  the  diaphragm 
down  and  a  similar  condition  below  the  diaphragm,  pushing  it  up.  It 
is  thus  apparent  that  subdiaphragmatic  abscess  is  a  typical  example  of 
what  is  known  as  the  border-line  case.  The  best  accounts  of  the  disease 
have  been  contributed  by  Rolleston4  and  Barnard.5 

1  Arch.' Radiology,  1915,  No.  131. 

2  Thesis,  Moscow,  1895. 

3  Revue  d.  Chirurgie,  1910,  xlii,  183  and  577. 
4Osler  and  McCeae:  "Modern  Medicine." 

5  Contributions  to  "Abdominal  Surgery,"  1910. 


DISEASES    OF   THE    DIAPHRAGM  597 

Etiology. — Clinically  two  types  are  recognized:  (1)  Simple  diaphrag- 
matic abscess,  and  (2)  a  gas-containing  abscess,  sometimes  referred  to 
as  subdiaphragmatic -pyopneumothorax  or  pyopneumothorax  subphren- 
icus  (Leyden) .  With  few  exceptions  the  primary  focus  of  infection  is  in 
the  abdomen  and  it  is  only  occasionally  that  the  abscess  has  its  origin 
above  the  diaphragm.  This  is  clearly  shown  in  the  combined  statistics 
of  Maydl,1  Grtineisen2  and  Perutz3  in  which  the  primary  source  was 
intrathoracic  in  but  18  out  of  448  cases.  Generally  speaking  any 
abdominal  lesion  may  give  rise  either  to  the  simple  or  to  the  gas-contain- 
ing type.  The  analysis  of  a  large  number  of  cases  has  shown,  however, 
that  certain  conditions  are  mainly  instrumental  in  forming  the  simple 
abscess  and  certain  other  conditions  are  most  apt  to  lead  to  the  gas- 
containing  type. 

The  most  frequent  cause  of  a  simple  abscess  is  appendicitis,  either  as 
a  complication  or  a  sequel.  In  a  small  percentage  of  cases  appendicitis 
is  associated  with  a  gas-containing  abscess.  Elsberg4  collected  75  cases 
of  subphrenic  abscess  following  appendicitis,  15  per  cent,  of  which  con- 
tained gas.  Next  to  appendicitis  the  most  important  factor  is  suppura- 
tion within  the  liver  itself.  This  may  be  a  suppurating  hydatid  cyst, 
an  amebic  abscess  or  infection  of  the  gall-bladder.  Among  the  less 
frequent  sources  of  infection  may  be  mentioned  retroperitoneal  or 
pericolic  abscess,  suppuration  in  or  about  the  pancreas,  or  the  Fallopian 
tubes,  and,  rarely  empyema,  pneumonia  or  trauma.  In  the  great  majority 
of  cases  the  simple  abscess  is  located  on  the  right  side  between  the  dia- 
phragm and  liver. 

The  gas-containing  abscess  has  a  different  and  less  varied  etiology. 
Here  the  most  frequent  cause  is  a  perforated  gastric  ulcer  and  to  a  less 
extent  a  perforated  duodenal  ulcer.  Perforation  of  a  gastric  cancer  or 
ulcer  in  the  colon  are  infrequent  causes.  The  gas-containing  abscess  is 
more  often  encountered  on  the  left  side  owing  to  the  frequency  of  gastric 
ulcer  as  a  predisposing  cause.  When  the  left  side  is  involved  the  dia- 
phragm forms  the  upper  and  posterior  boundary,  while  the  remainder  of 
the  wall  is  composed  of  some  part  or  -all  of  the  following  organs,  which 
are  commonly  matted  together:  stomach,  spleen,  transverse  colon  and 
left  lobe  of  the  liver. 

As  already  stated  the  conditions,  most  likely  to  produce  a  gas-con- 
taining abscess  may  cause  a  simple  abscess,  and,  in  like  manner,  the  con- 
ditions which  predispose  to  a  simple  abscess  may  give  rise,  occasionally,  to 
the  gaseous  type. 

A  subphrenic  abscess  is  always  unilateral,  as  the  falciform  ligament 
forms  a  natural  barrier.  The  condition  may  occur  at  any  age,  even  in 
very  young  children.  Jopson5  operated  on  a  child  fifteen  months  old 
in  whom  the  abscess  had  developed  secondarily  to  a  pneumonia. 

Lee6  has  reported  six  cases  of  subdiaphragmatic  inflammation.  The 
etiology  was  obscure  and  spontaneous  recovery  took  place  without  sup- 
puration. The  symptoms  and  physical  signs  were  those  occurring  in 
subdiaphragmatic  abscess. 

1  "Ueber  Subphrenische  Abscesse,"  1894. 

2  Arch.  f.  klin.  Chir.,  1903,  lxx,  1. 

3  Centralb.  f.  d.  Grenzgeb.  d.  Med.  u.  Chir.,  1905,  8. 

4  Annals  of  Surgery,  1901,  xxxiv,  729. 

5  Arch.  Pediatrics,  February,  1904. 

6  Jour.  Am.  Med.  Assoc,  April  17,  191.5. 


598  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

Morbid  Anatomy. — In  some  instances  the  abscess  may  be  considered 
as  a  localized  peritonitis.  As  a  rule,  the  wall  of  the  abscess  is  much  thick- 
ened, rough,  pouched  and  lined  with  necrotic  fibrin.  In  long-standing 
cases  the  deeper  layers  of  the  abscess  wall  show  cicatricial  tissue.  In  a 
few  instances  the  abscess  wall  is  smooth.  The  contents  may  consist  of 
pus  alone  or  pus  and  gas.  The  pus  may  be  thick  and  odorless  or  it  may  be 
mixed  with  blood,  bile  or  necrotic  tissue  and  have  a  fetid  odor.  If  the 
abscess  is  secondary  to  a  perforated  gastric  ulcer  it  also  may  contain 
particles  of  food.  The  size  of  the  abscess  varies  from  one  the  size  of  a 
hen's  egg  to  one  which  will  hold  one  or  two  pints.  Among  the  organisms 
found  in  the  pus  are  the  colon  bacillus,  streptococcus,  staphylococcus, 
bacillus  pyocyaneus,  pneumococcus,  tubercle  bacillus  and,  rarely,  the 
actinomyces. 

If  left  to  itself  a  subdiaphragmatic  abscess  often  perforates  the  dia- 
phragm and  in  this  way  sets  up  an  empyema  or  it  may  rupture  into 
the  lung  and  become  discharged  through  a  bronchus.  Rupture  into  the 
peritoneal  cavity  is  not  common.  Judd1  in  reporting  36  cases  from  the 
Mayo  Clinic  found  that  in  the  fatal  cases  extension  of  the  infection  to 
the  liver  and  the  formation  of  multiple  abscesses  was  the  most  frequent 
cause  of  death. 

A  subphrenic  abscess  may  arise  from  spread  of  the  infection  by  con- 
tiguity, as  in  the  case  of  a  liver  abscess;  by  way  of  the  blood  stream;  or 
through  the  lymphatics.  Posture  is  an  important  factor,  as. lymphatic 
drainage  in  the  abdomen  is  upward  through  the  diaphragm.  In  addi- 
tion the  subdiaphragmatic  space  is  a  natural  anatomical  pocket  when  the 
patient  is  in  the  recumbent  position,  hence  the  importance  of  gravity  in 
carrying  the  infection  to  this  point.  For  this  reason  the  adoption  of 
the  Fowler  position  by  surgeons  is  an  important  factor  in  prevention. 
Barnard  refers  to  a  case  in  which  the  primary  focus  of  infection  surrounded 
the  rectum.  The  infection  was  carried  by  way  of  the  lymphatics,  to  the 
left  subdiaphragmatic  space  where  it  localized  and  formed  an  abscess. 
It  then  ruptured  through  the  diaphragm  producing  an  empyema  and 
eventually  broke  into  the  lung  and  discharged  by  way  of  the  bronchi 
through  the  mouth. 

Symptoms. — The  onset  is  variable.  In  some  cases  it  is  sudden;  in 
others,  gradual  and  insidious.  Those  with  a  sudden  onset  are  usually  due 
to  a  perforated  gastric  ulcer.  In  such  cases  there  are  pain  and  tenderness 
in  the  left  upper  quadrant  of  the  abdomen,  vomiting  and  occasionally 
hiccough.  In  addition  the  patient  quickly  develops  the  symptoms  of 
suppuration — fever,  rapid  pulse,  quickened  breathing,  chills  and  sweat- 
ing. In  cases  with  an  insidious  onset  the  symptoms  due  to  the  abscess 
may  develop  so  gradually  that  they  may  be  attributed  to  the  primary 
condition.  In  the  majority  of  these  cases  the  first  symptom  is  pain  in 
the  lower  chest,  usually  on  the  right  side.  This  may  be  quite  severe  and 
radiate  to  the  shoulder  or  it  may  cause  but  little  discomfort.  Instead 
of  the  pain  there  may  be  a  feeling  of  tenderness  in  the  upper  abdominal 
quadrants.  All  who  have  given  much  attention  to  subdiaphragmatic 
abscess  emphasize  the  importance  of  suspecting  the  condition  in  indi- 
viduals with  indefinite  signs  and  symptoms  referable  to  the  lower  chest 
and  in  whom  the  symptoms  of  sepsis  are  more  pronounced  than  can  be 
accounted  for.  In  the  beginning  respiratory  symptoms  are  absent  or 
1  Journal-Lancet,  Minneapolis,  Nov.  15,  1915. 


DISEASES    OF    THE    DIAPHRAGM  599 

slight.  With  secondary  involvement  of  the  thorax  there  is  cough,  and 
the  respirations  may  be  irregular,  painful  or  rapid.  A  marked  leucocy- 
tosis  is  the  rule.  If  the  abscess  ruptures  through  the  diaphragm  and  into 
the  lung,  large  quantities  of  pus  may  be  spat  up,  as  in  the  case  of  pul- 
monary abscess.  If  the  abscess  is  not  drained,  surgically  or  otherwise., 
the  symptoms  of  sepsis  become  more  and  more  marked  and  the  patient 
finally  dies  from  exhaustion.  In  such  cases  the  duration  may  be  from  two 
to  three  months. 

Although  the  symptoms  usually  direct  attention  to  the  lower  chest 
or  upper  abdomen  they  rarely  indicate  the  location  of  the  trouble  with 
reference  to  the  diaphragm.  This  is  determined  by  physical  examina- 
tion and  more  particularly  by  the  X-rays. 

Physical  Signs. — The  physical  signs  are,  in  some  instances,  almost 
exclusively  thoracic;  in  others,  the  abdominal  signs  will  predominate; 
and  in  addition  they  will  vary  accordingly  as  the  abscess  is  simple  or 
gas-containing. 

Thoracic  Signs. — In  simple  abscess  the  location  is,  in  the  majority 
of  cases,  on  the  right  side  and  close  to  the  spinal  attachment  of  the 
diaphragm.  For  this  reason  the  physical  signs  will  be  found  over  the 
lower  and  posterior  aspect  of  the  right  lung.  There  is  diminished  ex- 
pansion on  the  right  side,  obliteration  of  the  intercostal  spaces  and  per- 
haps some  bulging  of  the  chest  wall.  Litten's  sign  should  be  looked  for. 
It  is  absent  in  cases  of  empyema  while  in  many  cases  of  subdiaphrag- 
matic abscess  it  is  present.  The  percussion  note  is  dull  and  the  upper 
limit  of  dulness  conforms  to  the  curve  of  the  dome  of  the  diaphragm. 
L'ee1  has  pointed  out  that  on  light  percussion  the  dulness  extends  as  high 
as  the  angle  of  the  scapula  while  on  deep  percussion  the  upper  limit  of 
dulness  is  much  lower.  In  addition  the  upper  limit  of  dulness  descends 
on  deep  inspiration.  Tactile  fremitus  is  usually  diminished.  On  auscul- 
tation the  breath  sounds  are  suppressed  or  absent  and  the  vocal  fremitus 
is  diminished.  Egophony  is  absent.  Occasionally  the  breathing  may  be 
bronchial  and  a  friction  rub  may  be  heard.  The  signs  are  not  distinctive 
and  can  readily  be  attributed  to  -a  pleural  effusion.  As  a  matter  of 
fact  they  may  be  due  to  an  effusion,  as  it  is  not  an  uncommon  complica- 
tion. Although  an  exploratory  puncture  is  of  service  in  determining 
the  presence  or  absence  of  fluid  the  most  valuable  evidence  as  to  the 
presence  of  a  subdiaphragmatic  abscess  is  furnished  by  the  X-rays. 
Examination  with  the  X-rays  shows  that  the  dome  of  the  diaphragm  on 
the  affected  side  is  pushed  up  by  a  dark  area  and  if  examined  with  the 
fluoroscope  the  movement  of  the  diaphragm  is  seen  to  be  much  restricted 
or  absent  (Fig.  354).  Even  in  cases  with  a  complicating  pleural  effu- 
sion the  outline  of  the  elevated  diaphragm  may  be  made  out. 

In  a  small  proportion  of  cases  a  simple  abscess  occurs  on  the  left  side. 
The  pulmonary  signs  are  the  same.  It  is  to  be  noted  that  the  displace- 
ment of  the  heart  is  not  marked  and  is  upward  rather  than  to  the  right 
as  in  cases  of  pleural  effusion.     Traube's  space  is  obliterated. 

Abdominal  Signs. — In  some  cases  the  signs  are  more  noticeably 
abdominal  although  thoracic  signs  may  be  present  also.  In  these  cases 
the  abscess  is  located  anteriorly  instead  of  posteriorly.  On  inspection 
there  is  seen  to  be  some  fulness  and  prominence  of  the  right  upper 
quadrant  and  the  epigastrium.     There  is  also  some  restriction  of  motion 

1  Loc.  oil. 


600  DISEASES    OF    THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

of  the  right  lower  chest.  Abdominal  swelling  due  to  subdiaphragmatic 
abscess  does  not  descend  with  inspiration  because  of  adhesions  (Barnard). 
The  skin  overlying  the  abscess  may  be  edematous  and  red  and  over  this 
area  fluctuation  may  be  obtained.  Pain  may  be  complained  of  in  the 
right  upper  quadrant  of  the  abdomen  and  on  pressure  tenderness  is 
usually  elicited.  If  the  pain  is  referred  from  the  chest  and  is  due  to 
pneumonia  or  pleurisy,  it  is  usually  superficial  in  character  and  not  in- 
creased by  deep  palpation  as  is  the  case  of  pain  which  is  abdominal  in 
origin.  There  is  usually  considerable  muscular  rigidity  in  the  epigas- 
trium and  right  upper  quadrant.     The  pain,  the  rigidity  and  the  bulging 


Fig.   354. — Subdiaphragmatic  abscess.     (Courtesy  of  Dr.  D.  R.  Boicen.) 

are  located  in  the  supraumbilical  region  while  the  lower  portion  of  the 
abdomen  remains  supple  (Dieulafoy).  The  use  of  an  exploring  needle 
should  be  resorted  to  early.  The  X-ray  findings  in  regard  to  the 
diaphragm  are  the  same  as  in  those  cases  in  which  the  thoracic  signs 
predominate. 

Signs  in  Gas-containing  Abscesses. — (Pyopneumothorax  subphren- 
icus). — Gas  may  be  present  from  the  onset  or  it  may  develop  later.  For 
this  reason  the  physical  signs  may  change.  Owing  to  the  frequency  of 
perforation  of  a  gastric  ulcer  as  the  exciting  cause  the  left  side  is  involved 
more  often  than  the  right.  The  physical  signs  may  simulate  those  of  a 
true  pneumothorax  very  closely  and  all  of  the  signs  peculiar  to  the  latter 
condition  may  be  present,  namely,  a  tympanitic  percussion  note,  amphoric 


DISEASES    OF    THE    DIAPHRAGM 


601 


breathing,  coin  test  and  succussion  splash.  The  following  points  may 
serve  to  distinguish  the  two  conditions :  The  percussion  note  is  tympan- 
itic in  the  upper  abdominal  quadrant  and  continues  upward  over  the 
chest.  It  never  extends  as  high,  however,  as  in  cases  of  true  pneumo- 
thorax. In  left-sided  cases  the  heart  is  not  much  displaced  to  the 
right  but  is  pushed  upward  in  the  case  of  an  abscess.  When  the  right 
side  is  involved,  the  liver  may  be  greatly  displaced  downward,  the  nor- 
mal hepatic  area  of  dulness  being  converted  into  tympany.  In  some  cases 
the  tympany  may  be  confined  to  the  area  behind  the  sternum.     Thoracic 


Fig.  355. — Growth  or  abscess  of  liver  rather  than  subdiaphragmatic  abscess,  since 
there  is  still  some  diaphragmatic  motion  and  owing  to  the  circumscribed  character  of  the 
elevation.     (Courtesy  of  Dr.  D.  R.  Bowen.) 


complications  are  almost  constantly  present.  A  pleural  effusion  often 
develops  and  in  the  beginning  may  be  serous.  The  use  of  an  exploratory 
needle  may  show  the  presence  of  a  serous  pleural  effusion  only.  The 
abdominal  signs  and  the  symptoms  of  sepsis  should  arouse  suspicion 
that  the  effusion  is  a  secondary  and  not  the  primary  trouble.  A 
pericardial  friction  rub  may  be  heard. 

Diagnosis. — Barnard  states  that  the  recognition  of  subdiaphragmatic 
abscess  will  be  facilitated  by  attention  to  the  following  points:  (I)  (a) 
A  history  of  diseases  which  may  produce  a  subphrenic  abscess;  (6)  the 
character  of  the  onset.  (II)  The  signs  and  symptoms  of  suppuration. 
(Ill)  Abdominal  signs  and  symptoms.     (IV)  Thoracic  signs. 


602         DISEASES    OF   THE   BRONCHI,    LUNGS,    PLEURA,    AND    DIAPHRAGM 

The  presence  of  a  subdiaphragmatic  abscess  is  always  a  possibility 
when  the  symptoms  and  signs  are  localized  in  the  lower  chest  or  upper 
portion  of  the  abdomen  or  both.  An  X-ray  examination  is  invaluable 
and  in  most  instances  will  distinguish  a  subdiaphragmatic  abscess  from 
conditions  which  give  rise  to  somewhat  the  same  signs.  At  times,  how- 
ever, the  question  may  arise  as  to  whether  the  bulging  of  the  diaphragm 
is  not  due  to  a  tumor  or  abscess  of  the  liver  itself  (Fig.  355). 


PART  IV 
DISEASES  OF  THE  PERICARDIUM,  HEART,  AND  AORTA 

By  H.  R.  M.  Landis,  A.  B.,  M.  D. 


CHAPTER  XXV 
DISEASES  OF  THE  PERICARDIUM 

ACUTE  FIBRINOUS  PERICARDITIS 

Etiology. — Inflammation  of  the  pericardium  is  rarely  primary;  it  oc- 
curs almost  without  exception,  as  a  secondary  lesion  or  as  a  complication 
in  some  other  disease.  It  is  commonly  encountered  in  association  with 
certain  of  the  acute  infections  (notably,  pneumonia,  acute  rheumatic  fever, 
tonsillitis,  or  scarlet  fever) ;  new  growths  or  ulcerative  processes  in  the 
esophagus,  vertebrae  or  bronchial  lymph  nodes;  and  finally  as  the  result 
of  trauma. 

In  tuberculosis  it  is  not  infrequently  encountered  either  as  part  of 
the  general  involvement  of  the  serous  surfaces,  or  as  an  independent  tu- 
berculous infection.  Wolff1  believes  that  a  tuberculous  origin  should 
be  suspected  in  all  cases  of  fibrinous  pericarditis  in  the  elderly  not  to  be 
explained  in  other  ways.  In  such  cases  the  pericarditis  is  either  not 
accompanied  by  demonstrable  tuberculosis  elsewhere  or  merely  by  healed 
lesions  in  the  apices.  As  a  complication  of  chronic  pulmonary  tuberculosis 
pericarditis  is  of  infrequent  occurrence.  Among  387  autopsies  at  the 
Phipps  Institute,  tuberculosis  of  the  pericardium  was  observed  but  3  times. 

In  the  chronic  diseases,  such  as  Bright's  disease,  diabetes  and  arterio- 
sclerosis a  terminal  pericarditis  is  not  infrequent;  it  is  usually  latent  and 
commonly  overlooked  during  life. 

Pericarditis  is  encountered  at  all  age  periods.  Males  are  attacked 
slightly  more  frequently  than  females. 

Morbid  Anatomy. — Acute  fibrinous  pericarditis  is  the  mildest  form  of 
the  disease.  It  is  sometimes  referred  to  as  dry  pericarditis,  although  there 
is  always  a  slight  excess  of  fluid  present.  This,  however,  is  not  demon- 
strable clinically.  The  affected  area  may  be  very  small,  or  it  may  include 
a  large  part  or  all  of  the  pericardial  surface.  The  inflammation  may 
manifest  itself  simply  as  a  lusterless,  roughened  spot  with  a  thin  fibrinous 
coating  which  is  readily  removed.  If  of  greater  severity  minute  granula- 
tions appear  on  the  surface  of  the  pericardium.  The  capillaries  are  injected 
and  proliferation  of  the  endothelial  and  connective-tissue  cells  is  set  up. 
In  addition  the  inflammatory  infiltration  penetrates  the  entire  depth  of 
the  membrane.  The  change  is  seen  most  frequently  at  the  base  of  the 
heart.  In  the  beginning  the  inflammatory  areas  are  patchy.  In  the 
severer  forms  these  patches  coalesce  and  the  fibrinous  coating  increases. 
1  Beiirage  z.  Klinik  der  Tuberculose,  1914,  xxx,  No.  1. 
603 


60-1  DISEASES    OF    THE    PERICARDIUM,    HEART,    AXD    AORTA 

In  extreme  cases  the  condition  presents  the  so-called  bread  and  butter 
appearance.  Under  these  circumstances  the  heart  presents  a  shaggy 
appearance,  sometimes  referred  to  as  hairy  heart  or  cor  viUosum  (Fig.  356). 

Symptoms. — Pericarditis,  in  all  forms,  is  notoriously  overlooked.  In 
the  acute  fibrinous  form  the  disease  is  apt  to  be  missed,  because  of  the 
small  area  over  which  the  friction  rub  is  audible.  This  can  be  avoided 
only  bv  a  painstaking  auscultatory  examination  of  the  precordial  region, 
in  the  presence  of  diseases  with  which  pericarditis  is  commmonly  associated. 
Another  factor  which  renders  the  recognition  of  the  acute  fibrinous  form 


Fig.  356. — Acute  serofibrinous  pericarditis.  The  pericardium,  which  was  opened  at 
the  bottom  has  been  reflected  upward  showing  both  the  visceral  and  the  parietal  surfaces, 
which  are  covered  with  thick  fibrinous  exudate,  the  thickness  of  which  can  be  seen  at  A,  at 
which  point  a  small  portion  of  the  pericardium  proper  is  exposed,  the  exudate  having  been 
scraped  away.  The  illustration  depicts  what  has  been  described  as  the  "  shaggy  heart." 
(From  the  Museum  of  the  Philadelphia  General  Hospital.) 

difficult  is  the  presence  of  marked  pulmonary  signs,  which  obscure  the 
murmur  produced  by  the  friction  rub.  This  is  particularly  true  in  cases 
of  croupous  pneumonia,  a  disease  which  shows  a  very  high  post-mortem 
percentage  of  involvement  of  the  pericardium.  This  discrepancy  between 
the  bedside  and  autopsy  findings  is  to  be  ascribed,  in  manyinstances,  to 
the  fact  that  acute  pericarditis  is  frequently  a  terminal  infection.  In  such 
cases  the  attention  is  so  centered  on  the  primary  affection  that  pains- 
taking physical  examinations  are  often  neglected. 

Pain  may  be  entirelv  absent,  or  it  may  be  of  a  very  sharp,  stabbing 


DISEASES    OF   THE    PERICARDIUM  605 

character.  It  is  usually  felt  over  the  heart  but  may  radiate  into  the 
abdomen  near  the  umbilicus,  to  the  left  side  of  the  neck  or  the  left 
shoulder.  It  is  often  increased  by  movement,  deep  breathing  or  cough- 
ing. Leaning  forward  in  bed  is  a  posture  often  assumed  by  patients 
suffering  from  inflammation  of  the  pericardium,  aortitis  or  mediastinal 
disease.  In  some  cases  tenderness  may  be  elicited  by  pressure  with  the 
finger-tips  in  the  region  of  the  apex.  In  place  of  the  pain  there  may  be  a 
feeling  of  oppression  or  tension  in  the  precorclium.  Slight  exertion  often 
produces  marked  rapidity  of  the  heart's  action,  and  irregularity  of  the 
cardiac  rhythm  is  common.  Pain  is  the  one  symptom,  however,  which 
can  be  said  to  belong  especially  to  pericarditis,  for  while  the  patient  usually 
has  fever  and  other,  evidences  of  a  more  or  less  severe  illness,  such  mani- 
festations belong- to  the  primary  trouble  rather  than  the  inflamed  peri- 
cardium. 

Physical  Signs. — Inspection  is  negative. 

Palpation. — This  is  also  negative  except  in  the  rare  instances  in  which 
a  friction  fremitus  is  felt. 

Percussion  shows  nothing  abnormal. 

Auscultation.— -If  the  condition  is  to  be  recognized  at  all  it  will  be  by 
auscultation,  although  just  as  in  inflammation  of  the  pleural  surfaces, 
there  may  be  no  evidence  of  a  friction  rub,  even  when  pain  is  marked. 
Furthermore,  while  a  friction  rub  may  b^  produced  by  the  slightest  degree 
of  inflammatory  change,  it  may  be  wanting  on  the  other  hand,  in  the 
presence  of  an  extensive  fibrinous  deposit. 

The  pericardial  friction  murmur  is  an  exocardial  murmur.  It  is  a 
double  or  to-and-fro  murmur,  accompanying  both  the  systolic  and  dias- 
tolic phases  of  the  heart.  The  quality  of  the  murmur  suggests  a  rubbing 
or  grazing  sound,  and  when  loud  is  apt  to  be  rough,  rasping  or  grating 
in  character.  The  sound  of  the  friction  may  be  intensified  by  having 
the  patient  lean  forward,  or  by  firm  pressure  of  the  stethoscope  over  the 
inflamed  area. 

Diagnosis. — A  pericardial  friction  rub  should  not  be  confounded  with  a 
single  endocardial  murmur,  or  with 'a  double  aortic  murmur.  While  it 
possesses  some  of  the  characteristics  of  a  double  aortic  lesion,  confusion 
can  be  avoided  if  it  is  kept  in  mind  that  the  friction  rub  is  limited  to  the 
precordial  area;  is  not  transmitted  as  are  the  aortic  murmurs;  and  arterial 
phenomena  are  absent.  Furthermore,  while  the  pericardial  murmur 
occurs  during  the  ventricular  phases  it  has  not  the  same  fixed  relation  to 
these  phases  as  has  the  double  aortic  murmur. 

Pleuro-pericardial  Friction  Murmur. — This  is  a  comparatively  com- 
mon condition  found  in  association  with  inflammatory  conditions  of  the 
pleura,  particularly  those  associated  with  pneumonia  and  tuberculosis. 
It  occurs  as  a  rule  along  the  left  border  of  the  heart,  and  is  caused  by  a 
roughened  inflamed  spot  on  the  pleura  coming  into'  contact  with  a  similar 
area  on  the  external  surface  of  the  pericardium.  In  some  cases  the  pain 
produced  by  this  condition  is  intense.  This  murmur  may  occur  during 
but  one  phase  of  the  heart,  or  it  may  be  to-and-fro.  The  intensity  of  the 
sound  varies  greatly,  because  it  is  influenced  by  the  respiratory  move- 
ments of  the  lungs.  Holding  the  breath  or  taking  a  deep  inspiration  may 
cause  it  to  disappear  entirely.  It  is  loudest  when  that  particular  period 
of  the  respiratory  phase  brings  the  two  inflamed  surfaces  momentarily 
together. 


606 


DISEASES    OF    THE    PERICARDIUM,    HEART.    AND    AORTA 


TUBERCULOUS   PERICARDITIS 

The  origin  of  this  form  of  the  disease  is  not  clear.  Infection  bjr  the 
blood  stream  seems  the  most  probable  because  of  this  mode  of  transmis- 
sion in  other  viscera.  Extension  of  the  disease  by  contiguity  cannot  be 
considered  a  factor  of  much  importance  in  view  of  the  relative  infre- 
quency  of  the  disease  in  association  with  chronic  pulmonary  tuberculosis. 
Extension  of  the  disease  by  way  of  the  lymphatics  is  open  to  the  same 
objection.  Any  of  the  anatomical  forms  of  pericarditis  may  be  produced 
by  tuberculosis.  In  the  acute  form  there  may  be  a  fibrinous,  a  sero- 
fibrinous, a  hemorrhagic  or  a  purulent  exudate. 


Fig.  357. — Tuberculous  pericarditis. 


In  the  chronic  form  the  pericardium  may  be  thickened  and  studded 
with  tubercles  (Fig.  357) .  In  other  instances  the  pericardium  is  greatly 
thickened,  adherent  and  contains  varying-sized  pockets  of  caseous  mate- 
rial. In  some  instances  a  distinct  line  of  caseous  material  may  mark  the 
line  of  junction.  In  the  chronic  adhesive  type  of  pericarditis,  tubercle 
formation  is  not  a  marked  feature.  Everything  points  to  a  chronic 
inflammatory  condition  in  which  the  tubercle  bacillus  has  played  but  a 
small  part.  Furthermore,  the  chronic  adhesive  type  often  occurs  in 
frankly  tuberculous  subjects  with  no  gross  or  histological  evidence  of 
tuberculosis  in   the   pericardium.     Brooks  and  Lippencott1  state  that 

1  Am.  Jour.  Med.  Sc,  December,  1909. 


DISEASES    OF    THE    PERICARDIUM 


607 


among  61  instances  of  chronic  adhesive  pericarditis,  tuberculosis  was  the 
apparent  etiological  factor  in  17.  In  none  of  them,  however,  were  tuber- 
culous lesions  present  in  the  pericardium,  the  change  apparently  being  due 
to  the  toxemia  of  the  disease  rather  than  from  direct  action  of  the  tubercle 
bacillus.  Norris1  found  82  cases  of  tuberculous  pericarditis  among  7219 
general  autopsies,  1780  of  which  were  autopsies  on  clinically  tuberculous 
individuals. 

PERICARDIAL  EFFUSION 

Fluid  within  the  pericardial  sac  sufficient  to  be  designated  an  effusion 
may  succeed  simple  fibrinous  pericarditis.  Under  these  circumstances 
the  symptoms  at  the  onset  are  identical  with  the  fibrinous  form.  In 
other' instances  there  are  no  initial  symptoms  and  the  effusion  gives  no 
hint  as  to  its  presence  until  it  has  attained  such  proportions  as  to  produce 
pressure  symptoms  and  cardiac  embarrassment,  The  latent  forms  are  not 
infrequently  tuberculous  or  renal  in  origin,  while  those  with  a  frank  onset 
are  commonly  associated  with  rheumatic  fever,  pneumonia  or  septicemia. 


Fig.  358, 


-Hydropericardium. 
4,  Liver. 


1,  Esophagus.     2,  Aorta.     3,  Inferior  vena  cava. 
5,  Heart.      (After  Pirogoff.) 


Hemopericardium. — Actual  hemorrhage  into  the  pericardium  may  be 
due  to  a  stab  or  gunshot  wound,  a  ruptured  blood-vessel,  one  of  the  hem- 
orrhagic diseases,  malignant  disease  of  the  mediastinum  or  tuberculosis. 
Norris  found  16  cases  of  hemopericardium  among  8640  autopsies  at  the 
Philadelphia  Hospital.  Clear  blood  was  found  in  the  pericardium  in  3  of 
197  cases  of  tuberculosis  autopsied  at  the  Phipps  Institute. 

Hydropericardium. — A  marked  increase  in  the  amount  of  the  peri- 
cardial fluid  is  often  encountered  in  conditions  associated  with  failure  of 
the  circulation.  It  is  not  due  to  inflammation  but  is  a  transudate  and  is, 
as  a  rule,  associated  with  effusions  into  the  other  serous  cavities  (Fig. 
358). 

Morbid  Anatomy. — To  the  lesions  found  in  the  acute  fibrinous  form  is 
added  an  excessive  amount  of  fluid,  which  may  be  serofibrinous,  purulent 
or  hemorrhagic  in  character.  The  primary  disease  in  the  serofibrinous 
1  Norris,  G.  W.,    Univ.  of  Pa.  Med.  Bull,  July-Aug.,  1904. 


608  DISEASES    OF   THE    PERICARDIUM,    HEART,    AND   AORTA 

form  is  usually  rheumatic  fever  or  pneumonia;  in  the  hemorrhagic  form, 
tuberculosis,  Bright's  disease,  malignant  disease  or  scurvy;  if  purulent  in 
character  scarlet  fever,  pneumonia,  tuberculosis,  or  some  septic  condition 
such  as  puerperal  fever,  is  the  exciting  cause  (see  Fig.  175). 

Symptoms. — If  the  effusion  supervenes  upon  an  attack  of  acute  fibrin- 
ous pericarditis  its  recognition  is  sometimes  facilitated  by  the  history  of 
precordial  pain  and  the  presence  of  a  friction  rub.  If,  however,  pain  has 
been  wanting,  and  the  friction  rub  has  escaped  detection,  or  the  effusion 
has  developed  insidiously,  as  not  infrequently  happens  in  tuberculous 
cases  or  Bright's  disease,  its  detection  is  notoriously  uncertain.  In  the 
presence  of  one  of  the  commoner  etiological  factors,  such  as  acute  rheuma- 
tism or  acute  croupous  pneumonia,  the  gradual  evolution  from  a  dry 
fibrinous  pericarditis  to  pericarditis  with  effusion  may  be  traced  readily. 
If,  however,  the  case  is  seen  after  the  effusion  has  taken  place,  as  com- 
monly happens,  the  recognition  of  the  condition  is  extremely  difficult. 
It  is  probably  no  exaggeration  to  state  that  more  instances  of  this  type 
escape  recognition  than  are  correctly  diagnosed. 

In  the  absence  of  pain,  dyspnea  is  perhaps  the  most  important 
symptom.  If  the  dyspnea  is  associated  with  pressure  symptoms,  atten- 
tion may  be  directed  to  the  pericardium,  otherwise  the  heart  itself  will  be 
believed  to  be  the  cause  of  the  respiratory  distress.  In  addition  to  the 
dyspnea  pressure  exerted  by  the  distended  pericardial  sac  may  manifest 
itself  by  cyanosis  of  the  face,  distention  of  the  veins  of  the  neck,  a  rapid, 
small  and  irregular  pulse,  dysphagia,  aphonia  and  an  irritating  cough. 
It  can  be  seen  that  there  is  nothing  pathognomonic  in  these  symptoms,  and 
that  a  similar  picture  is  produced  by  other  conditions.  Restlessness  and 
insomnia  are  commonly  present,  and  in  addition  mental  symptoms 
have  been  noted. 

Physical  Signs. — Unless  the  effusion  has  reached  a  considerable 
amount,  probably  not  less  than  half  a  pint,  its  recognition  by  physical 
signs  is  hardly  possible,  even  when  there  is  every  reason  to  believe  that 
such  a  condition  may  exist.  The  physical  signs  as  given  below  relate  to  a 
large  collection  of  fluid  within  the  sac. 

Inspection. — An  individual  suffering  from  a  pericardial  effusion  suf- 
ficient to  embarrass  the  heart's  action  is  apt  to  present  an  anxious  expres- 
sion, some  duskiness  of  the  face  and  difficulty  in  breathing.  The  latter  is 
manifested  by  the  rapid  and  labored  character  of  the  respirations  and 
the  posture.  The  patient  seeks  relief  of  his  respiratory  distress  by  having 
the  upper  part  of  the  body  raised,  or  by  sitting  up  and  leaning  forward. 

In  children  a  noticeable  bulging  in  the  precordial  region  is  often  to  be 
observed.  In  adults,  however,  this  is  rarely  the  case,  although  careful 
inspection  may  reveal  some  fulness  of  the  intercostal  interspaces  (third 
and  fourth)  and  possibly  an  undue  prominence  in  the  epigastric  region. 
Edema  of  the  chest  wall  may  be  present  if  the  effusion  is  purulent. 

The  apex  beat  of  the  heart  is  either  absent  or  the  cardiac  impulse  is 
indistinct,  and  seen  only  in  the  third  and  fourth  interspaces  to  the  left. 

If  the  effusion  attains  any  considerable  size,  it  so  fills  the  thoracic 
cavity  as  to  cause  compression  of  the  left  lung,  this  being  apparent  from 
the  diminished  expansion  of  the  left  chest  (Fig.  359). 

Palpation. — Pressure  may  show  the  presence  of  a  localized  edema. 
The  apex  beat  of  the  heart  may  be  located  in  its  normal  position,  or  it  may 
be  felt  in  the  fourth  interspace,  especially  in  children.     The  friction 


DISEASES    OF   THE    PERICARDIUM 


609 


rub  or  part  of  it  may  persist  at  the  base,  and  be  felt  on  palpation.  Fluc- 
tuation is  practically  never  detected.  Some  observers  have  emphasized 
the  importance  of  the  pulsus  paradoxus  in  association  with  pericardial 
effusion.  Such  a  pulse  is  small,  usually  rapid  and  during  each  inspiration 
the  pulse  becomes  much  weaker,  or  is  entirely  lost  at  the  wrist. 

Percussion. — -If  a  pericardial  effusion  is  to  be  recognized  by  physical  signs 
it  will  be  through  the  percussion  findings.  It  is  to  be  borne  in  mind  that 
the  pericardium  is  a  fibro-serous  sac  which  envelops  the  heart;  that  it  is 
somewhat  pyramidal  in  shape,  resting  on  the  diaphragm  to  which  it  is 
attached,  and  that  above  it  merges  into  the  external  coats  of  the  aorta  and 
pulmonary  artery  at  the  root  of  the  heart.     In  the  greater  part  of  its  ex- 


Fig.  359. — Serous  pericarditis.  1,  Esophagus. _  2,  Descending  aorta.  3,  Right  auricle. 
4,  Right  ventricle.     5,  Left  auricle.     6,  Left  ventricle. 

The  left  auricle  is  compressed  by  the  pericardial  exudate.  The  antero-posterior  diame- 
ter of  the  whole  chest  is  increased.  The  heart  is  turned  on  its  axis  and  lies  more  horizon- 
tally than  is  normally  the  case.  The  lungs  are  somewhat  compressed  and  pushed  far 
back  from  the  anterior  pericardial  surface  which  they  normally  cover.  The  pleural  sacs, 
however,  retain  their  normal  position,  a  fact  which  is  of  importance  in  regard  to 
paracentesis  pericardii.     (After  Pirogoff.) 

tent,  it  is  separate  from  the  anterior  wall  of  the  thorax  by  the  anterior 
margins  of  the  lung  and  pleural  sacs,  but  is  in  direct  relation  with  the  left 
half  of  the  lower  portion  of  the  body  of  the  sternum. 

If  a  large  excess  of  fluid  is  poured  out  into  the  sac,  either  in  the  form  of 
an  exudate  or  transudate,  the  sac  distends,  and  extends  beyond  its  nor- 
mal limits.  And  in  proportion  to  the  distention  the  precordial  area  be- 
comes correspondingly  more  pyramidal  in  shape,  the  base  being  below 
and  the  apex  at  the  third  interspace  to  the  left  of  the  sternum.  This  is 
largely  due  to  the  fact  that  the  sac  as  it  increases  in  size  pushes  aside  the 
anterior  portions  of  the  lungs  which  normally  cover  the  major  portion  of 
the  pericardium.  The  transverse  diameter  is  greatest  at  the  fourth  or 
fifth  interspace.  Dulness  extending  1  to  2  inches  to  the  right  of  the  ster- 
num is  of  considerable  importance,  and  is  known  as  Rotch's  sign.  In 
addition  to  the  increase  in  the  transverse  diameter  and  the  extension  of 

39 


610  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

dulness  to  the  right,  the  area  of  dulness  may  extend  to  the  left,  beyond 
the  apex  beat;  while  theoretically  the  latter  condition  is  possible  and 
often  mentioned  as  occurring,  it  is  rarely  noted  (see  Figs.  216-217). 

If  the  effusion  is  very  large,  compression  of  the  left  lung  may  be  mani- 
fested in  two  ways:  (1)  by  a  high-pitched  tympanitic  percussion  note  in 
the  left  axillary  region;  and  (2)  by  an  area  of  dulness  posteriorly  just 
beneath  the  angle  of  the  left  scapula.  The  latter  may  be  increased  or 
diminished  accordingly  as  the  patient  sits  up  or  leans  forward. 

Auscultation. — Unless  the  original  friction  rub  has  been  heard  all 
over  the  precordium,  or  has  been  limited  to  the  base  of  the  heart,  it 


Fig.  360. — Pericardial  effusion.      Pleural  effusion.    (Courtesy  of  Dr.  D.  R.  Bowen.) 

disappears  with  the  appearance  of  the  fluid  which  separates  the  parietal 
and  visceral  layers.  In  the  absence  of  a  friction  rub  the  only  noteworthy 
auscultatory  finding  is  the  muffled  and  distant  character  of  the  heart 
sounds  at  the  apex,  and  over  the  body  of  the  heart.  The  intensity  of  the 
heart  sounds  may  be  altered  by  posture,  being  more  audible  in  the  erect 
than  in  the  recumbent  position.  In  addition  to  rapidity  of  the  cardiac 
action,  a  disturbance  of  the  rhythm  and  accentuation  of  the  pulmonic 
second  sound  are  frequently  encountered.  Inasmuch  as  the  exciting- 
cause  of  endocarditis  is  often  the  same  as  that  producing  pericarditis 
the  presence  of  an  endocardial  murmur  may  add  to  the  difficulties  of 
diagnosis. 


DISEASES    OF    THE    PERICARDIUM  611 

Another  associated  condition  which  makes  the  recognition  of  pericar- 
dial effusion  a  difficult  matter  is  croupous  pneumonia,  involving  the  left 
lung.  Under  these  circumstances  two  factors  aid  in  obscuring  the 
secondary  condition;  first,  the  symptoms  referable  to  the  pulmonary 
affection ;  and  secondly,  the  physical  signs. 

Diagnosis. — Aside  from  entirely  overlooking  the  presence  of  fluid  in 
the  pericardial  sac,  the  next  most  common  error  is  in  mistaking  the  con- 
dition for  cardiac  dilatation.  And  while  the  distinction  between  the  two 
conditions  is  theoretically  easy,  their  differentiation  at  the  bedside  is 
often  a  difficult  matter.  In  weighing  the  evidence  it  should  be  remem- 
bered that  in  dilatation  the  apex  beat  is  visible  and  diffuse;  the  area  of 
dulness  is  an  exaggeration  of  the  normal  triangular  space  and  does  not 
assume  the  pear-shaped  area  seen  in  effusion,  nor  does  it  alter  the  per- 
cussion note  over  the  left  lung;  the  heart  sounds  are  distinct,  valvular 
or  fetal  in  character,  and  gallop  rhythm  is  common.  If  the  patient  is 
stout  and  the  chest  wall  thick,  the  points  of  difference  in  favor  of  cardiac 
dilatation  are  greatly  obscured. 

Because  of  the  strong  cardiac  impulse  and  intensity  of  the  heart 
sounds  simple  hypertrophy  of  the  heart  should  cause  no  confusion. 

An  encysted  collection  of  fluid  between  the  lobes  of  the  lungs,  or  in 
the  pleural  sac  may  simulate  a  pericardial  effusion.  The  differentiation 
will  rest  largely  on  the  character  of  the  physical  findings. 

A  tumor  in  the  anterior  mediastinum  may  approximate  the  area  of 
dulness  occurring  in  a  pericardial  effusion.  An  example  of  this  is  shown 
in  Fig.  307. 

The  X-ray  is  the  most  certain  means  of  detecting  a  pericardial  effusion 
and  in  doubtful  cases  should  be  resorted  to  whenever  possible  (Fig.  360). 

ADHESIVE  PERICARDITIS 

Etiology. — Chronic  adhesive  pericarditis  may  be  the  final  stage  of  the 
acute  fibrinous  form,  although  it  rarely  falls  to  the  lot  of  any  one  observer 
to  follow  this  change.  The  adherent  type  is  most  frequently  encountered 
years  after  the  initial  mischief,  and  almost  invariably  presents  itself 
in  some  form  of  cardiac  embarrassment.  Acute  rheumatic  fever  is  the 
most  frequent  predisposing  cause.  In  the  absence  of  a  history  of  this 
infection,  tuberculosis  seems  to  be  the  next  most  important  factor.  A 
tuberculous  origin  of  the  trouble  is  to  be  suspected,  especially  if  the 
patient  presents  any  evidence  of  tuberculosis,  either  latent  or  active. 
Brooks  and  Lippencott1  in  a  study  of  1000  protocols  found  150  instances 
of  pericarditis,  61  of  which  were  of  the  chronic  adhesive  type.  Of  these 
61  cases  tuberculosis  was  the  apparent  etiological  factor  in  17.  Hoist2 
found  evidences  of  adhesive  pericarditis  in  61  cases  among  1586  autopsies. 
Tuberculosis  was  present  in  10  of  the  61  cases  (see  "Tuberculous  Peri- 
carditis," p.  606).  Sicard  among  2000  autopsies  found  adhesive  peri- 
carditis in  77  instances.  The  condition  may  be  expected,  therefore,  in 
about  4  per  cent,  of  all  cases  coming  to  autopsy. 

Morbid  Anatomy. — Several  varieties  of  adhesive  pericarditis  are  en- 
countered. (1)  The  adhesions  may  obliterate  only  a  portion  of  the  peri- 
cardial sac  (see  Fig.  218).     (2)   Obliteration  of  the  sac  may  be  complete 

1  .1//;.  Jour.  Med.  Sc,  December,  1909. 

-  Xorsl;  Magazin  for  Lae<j<  riili  iisLoIk  it.  October,  1914,  lxxv. 


612  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


Fig.  361.- — Chronic  adhesive  pericarditis. 


Fig.  362. — Mediastino-pericarditis. 


DISEASES    OP    THE    PERICARDIUM  613 

(Fig.  361).  (3)  The  sac  may  be  obliterated  and  in  addition  is  adherent 
to  surrounding  structures  (mediastino-pericarditis)  (Fig.  362).  (4)  As  a 
part  of  a  multiple  serositis.  When  old  the  fibrous  tissue  is  dense  and 
tough  and  cannot  be  separated  from  the  heart  without  tearing  the  latter. 
When  adherent  to  the  surrounding  structures  the  heart,  lungs  and 
mediastinal  contents  cannot  be  separated  and  must  be  removed  en  masse. 

The  heart  muscle  itself  is  apt  to  present  degenerative  changes  and 
there  is  very  commonly  an  associated  endocarditis.  In  common  with 
aortic  insufficiency  and  general  arterio-sclerosis,  adhesive  pericarditis 
often  produces  the  most  extreme  degree  of  cardiac  Irypertrophy  met 
with.  When  symptoms  do  arise  they  are  usually  due  to  myocardial 
changes  which  may  have  developed  concomitantly  with  the  pericardial 
damage  or  independently. 

Pathological  Physiology. — The  mechanical  effects  upon  the  circula- 
tion due  to  the  adhesions  are  described  by  Hirschfelder  as  follows:  (1) 
The  work  of  the  ventricle  is  increased  by  the  tug  upon  the  adhesions. 
(2)  The  filling  of  the  heart  may  be  hindered  by  strangulation  of  the  vena 
cava.  At  each  contraction  the  heart  must  not  only  drive  out  the  blood, 
but  must  pull  on  its  harness  of  adhesions.  The  additional  work  will 
depend  on  the  tightness  of  the  adhesions  and  the  weight  and  rigidity  of 
the  structures  pulled.  Adhesions  between  the  ribs  and  diaphragm 
cause  the  greatest  effort.  (3)  The  emptying  of  the  heart  and  the  flow 
through  the  aorta  may  be  hindered  by  the  tugging  of  adhesions  upon  the 
arch  of  the  aorta. 

As  the  result  of  the  increased  work  the  heart  hypertrophies  just  as 
it  does  in  the  presence  of  chronic  endocarditis.  As  degenerative  changes 
are  relatively  common  in  the  heart  muscle,  either  as  the  result  of  the 
fibrosis  extending  in  from  the  pericardium  or  as  an  independent  affection, 
compensation  is  apt  to  fail  if  the  heart  is  subjected  to  an  undue  strain. 
When  compensation  fails,  it  may  present  the  clinical  picture  of  failure  of 
the  left  ventricle  with  marked  dyspnea  or  pulmonary  edema;  or  it  may 
manifest  itself  chiefly  by  the  signs  of  venous  stasis  such  as  occur  in  failure 
of  the  right  ventricle.  Hirschfelder  states  that  the  type  of  broken  com- 
pensation will  depend  on  whether  the  adhesions  are  greatest  over  the 
left  or  over  the  right  ventricle. 

Death  is  seldom  clue  to  the  pericarditis  itself.  It  occurs  either  as  the 
result  of  degenerative  changes  in  the  heart  muscle  or  to  exhaustion  of 
the  heart  as  the  result  of  some  intercurrent  affection. 

The  relative  frequency  of  the  condition  and  the  fact  that  it  is  encoun- 
tered far  more  often  at  the  autopsy  table  than  during  life  indicate  that, 
except  under  unusual  circumstances,  the  lesion  is  not  of  great  importance. 

Symptoms. — There  are  no  symptoms  which  suggest  the  presence  of 
adherent  pericarditis.  In  what  has  been  designated  as  the  silent  group, 
the  existence  of  adhesive  pericarditis  escapes  notice  entirely  as  there  are 
neither  symptoms  nor  signs  referable  to  the  heart. 

In  the  group  in  which  the  ill  health  is  obviously  cardiac  in  origin  the 
recognition  of  adhesive  pericarditis  will  depend  largely  on  the  thorough- 
ness of  the  physical  examination.  If  it  is  assumed  that  the  hypertrophy 
or  dilatation  of  the  heart  is  purely  cardiac  in  origin,  or  that  it  is  secondaiy 
to  vascular  or  renal  disease,  the  true  cause  will  not  be  suspected.  Fur- 
thermore, it  only  too  frequently  happens  that  in  addition  to  the  adherent 
pericardium  there  is  also  an  endocarditis.     Under  these  circumstances 


614  DISEASES    OF   THE    PERICARDIUM,    HEART,    AND    AORTA 

it  is  usually  taken  for  granted  that  the  endocarditis  is  the  only  condition 
present.  Whether  cardiac  murmurs  are  present  or  not,  adhesive  peri- 
carditis is  to  be  thought  of  in  a  young  adult  if  there  is  a  history  of  acute 
rheumatic  fever  followed  by  endocarditis,  and  especially  so  if  the  cardiac 
failure  is  more  marked  or  the  cardiac  enlargement  more  extensive  than 
the  endocardial  damage  seems  to  warrant.  An  additional  point  of  some 
importance  is  the  fact  that  in  young  individuals  apparently  suffering 
from  endocarditis,  an  adherent  pericardium  is  to  be  suspected  when  the 
heart  does  not  respond  to  digitalis. 

The  recognition  of  adhesive  pericarditis  seems  to  be  as  uncertain  to- 
day as  it  was  a  century  ago.  Corvisart1  expressed  the  diagnostic  diffi- 
culties as  follows:  "From  its  insensible  attack,  from  its  secret  progress, 
arises  in  most  cases  a  difficulty  often  insurmountable  in  the  diagnosis 
of  this  inflammation.  If  we  attend  to  the  few  observations  transmitted 
to  us  on  this  point  of  practice,  we  know  not  by  what  signs  to  distinguish 
its  attack,  what  symptoms  accompany  its  progress ;  hence  we  are  obliged 
to  grant  that  all  the  phenomena  that  belong  to  this  disease  are  so  vague, 
that  it  is  even  uncertain  whether  a  combination  of  a  great  number  of 
observations  of  this  kind  can  throw  much  light  on  its  history."  Gee  has 
expressed  the  opinion  that  in  the  discovery  of  adherent  pericardium  we 
seldom  get  farther  than  a  guess. 

Physical  Signs. — Inspection. — It  is  doubtful  whether  a  diagnosis  of 
adherent  pericarditis  can  be  made  unless  systolic  retraction  of  the  inter- 
spaces is  present.  The  retraction  is  systolic  in  time  an"(f~occurs  in  the 
region  of  the  apex.  Systolic  retraction  also  should  be  looked  for  poste- 
riorly on  the  left  side  between  the  eleventh  and  twelfth  ribs  (Broadbent's 
sign).  In  extreme  cases  the  costal  cartilages  or  xyphoid  cartilage  may 
be  pulled  in  with  each  systole.  Epigastric  systolic  retraction  is  a  normal 
phenomenon  and  must  not  be  confused  with  the  aforementioned  forms. 

The  character  of  the  cardiac  impulse  is  not  of  much  value  as  it  re- 
sembles that  encountered  either  in  hypertrophy  or  dilatation  of  the  heart. 
Diastolic  collapse  of  the  cervical  veins  is  cited  as  an  evidence  of  adherent 
pericarditis,  but  it  is  a  sign  of  relatively  little  value. 

Palpation. — The  most  notable  finding  on  palpation  is  the  presence  of 
diastolic  shock.  This  sign  ranks  with  systolic  retraction  as  being  the 
most  important  evidence  of  the  existence  of  obliterative  pericarditis. 
The  pulsus  paradoxus  is  commonly  present,  but  its  diagnostic  value  is 
relatively  unimportant . 

Percussion. — If  the  pericarditis  is  also  associated  with  a  medias- 
tinitis,  percussion  may  show  that,  the  anterior  margin  of  the  left  lung  is 
immovable  and  does  not  change  with  inspiration  and  expiration.  The 
normal  lateraJjnpJDili^  of  posture,  does  not 

occur.  "~  ' 

"—Auscultation. — There  are  no  auscultatory  signs  distinctive  of  adhesive 
pericarditis.  As  has  been  already  pointed  out  endocardial  murmurs  may 
be  present.  If  they  are,  it  is  to  be  borne  in  mind  that  they  do  not  vitiate 
a  [diagnosis  of  adherent  pericardium  inasmuch  as  the  association  is  a 
frequent  one.  Among  46  cases  in  which  a  presystolic  apical  murmur 
occurred  without  mitral  stenosis,  Phear2  found  that  20  were  associated 

'"Essay  on  Organic  Diseases  of  the  Heart  and  Great  Vessels,''  Eng.  Trans,  bv 
Gates,  1812. 

2  Lancet,  1895,  ii,  716. 


DISEASES    OF   THE    PERICAEDIUM  615 

with  adhesive  pericarditis.  The  explanation  which  has  been  offered  to 
explain  this  murmur  is  that  vibrations  may  be  set  up  by  the  current  pro- 
pelled from  a  dilated  and  hypertrophiecl  auricle  into  a  ventricle  whose 
muscular  walls  are  deficient  in  tone. 

Auscultation  of  the  lungs  may  reveal  bronchovesicular  breathing  at 
the  left  scapular  angle  due  to  compression  of  the  lung. 

Pick's  Disease  or  Pericardial  Pseudo-cirrhosis  of  the  Liver. — When 
in  addition  to  the  pericardium,  the  mediastinum,  pleura,  liver  and  omen- 


Fig.  363. — Chronic  adhesive  pericarditis.  This  specimen  illustrates  the  "  Zuckerguss- 
herz,"  so  called  owing  to  the  resemblance  of  the  exudate  to  the  sugar  icing  on  a  cake.  It 
is  generally  met  with  in  association  with  "pericardial  pseudocirrhosis  of  the  liver."  (Speci- 
men from  the  German  Hospital,  Philadelphia.) 

turn  are  also  involved,  we  have  what  has  been  described  as  pericardial 
pseudo-cirrhosis  of  the  liver,  or  Pick's  disease.  The  heart  and  liver  are 
covered  with  a  thick  white  layer  of  inflammatory  product,  giving  them 
the  appearance  of  being  coated  with  an  "icing,"  hence  the  German  name 
"Zuckerguss  Leber  and  Herz"  (Fig.  363).  The  condition  is  often 
tuberculous  in  origin.  Head  has  collected  55  cases  from  the  literature  and 
added  4.     This  symptom-complex,  sometimes  called  multiple  serositis, 


616  DISEASES    OP   THE    PERICARDIUM,    HEART,    AND   AORTA 

presents  the  clinical  picture  of  cirrhosis  of  the  liver.  Ascites  and  dropsy 
of  the  lower  extremities  are  the  most  prominent  signs  while  the  upper  part 
of  the  body  remains  free  from  edema.  Jaundice  is  absent  or  very  tran- 
sient in  character,  and  aside  from  the  ascites  there  is  no  other  evidence 
of  portal  obstruction.  Dyspnea  and  engorgement  of  the  veins  of  the 
neck  are  usually  present  in  Pick's  disease,  but  the  frequency  of  asso- 
ciated cardiorenal  disease  in  true  cirrhosis  is  apt  to  produce  the  same 
phenomena. 

The  recognition  of  this  condition  will  depend,  almost  entirely  on  the 
detection  of  the  signs  indicative  of  adhesive  pericarditis.  If  such  signs 
are  present  the  diagnosis  is  possible,  otherwise  the  assumption  is  certain 
to  be  that  of  cirrhosis  of  the  liver  as  the  cause  of  the  trouble. 


CHAPTER  XXVI 
DISEASES    OF   THE   MYOCARDIUM 

Introduction. — Valvular  disease  of  the  heart  is,  with  few  exceptions, 
easily  determined.  Changes  in  the  heart  muscle,  on  the  other  hand,  are 
often  extremely  difficult  to  recognize.  Although  the  term  "  heart  dis- 
ease" is,  in  the  minds  of  many,  associated  with  a  valvular  defect  it  can- 
not be  too  strongly  emphasized  that  the  ability  of  the  heart  to  carry 
on  its  functions  is  dependent,  almost  entirely,  on  the  condition  of  the 
cardiac  muscle.  The  majority  of  valvular  defects  are  for  a  long  time,  and, 
in  some  instances  always,  of  secondary  importance.  So  long  as  the 
cardiac  muscle  remains  healthy,  the  heart,  subject  to  chronic  valvular 
disease  is  capable  of  performing  its  work  as  effectively  as  a  normal  heart. 
It  is,  of  course,  understood  that  such  a  heart  is  functionally  normal  under 
ordinary  conditions ;  it  cannot  often  withstand  unusual  demands.  When, 
however,  the  heart  muscle  becomes  exhausted  as  the  result  of  compensa- 
tion having  reached  its  limit  or  when  the  muscle  becomes  impaired 
through  degenerative  changes,  with  or  without  a  valvular  defect,  the 
most  serious  circulatory  disturbances  take  place.  The  diagnosis  of 
structural  changes  in  the  heart  muscle  is  often  beset  with  difficulty. 
Hypertrophy  of  the  heart  is,  as  a  rule,  easily  recognized;  so  too  is  the 
dilatation  which  succeeds  hypertrophy.  Degenerative  changes,  on  the 
other  hand,  are  often  entirely  overlooked  although  the  etiological  factor 
should,  in  many  instances,  put  us  on  our  guard.  This  is  particularly 
true  in  cases  of  diphtheria  where  it  is  well  recognized  that  acute  degenera- 
tive changes  in  the  muscle  are  relatively  common  and  may  end  fatally 
unless  the  possibilities  of  such  a  lesion  is  recognized.  Broadbent  has  stated 
the  case  very  clearly.  "Too  commonly  no  attempt  is  made  to  recognize 
the  existence  and  extent  of  degeneration  or  dilatation.  The  symptoms 
due  to  derangement  of  the  circulation  force  themselves  upon  the  atten- 
tion of  the  medical  man,  but  no  murmur  being  detected,  the  only  diag- 
nosis ventured  upon  is  that  of  'weak  heart,'  a  vague  term  which  covers 
the  entire  ground,  from  temporary  functional  debility  to  disease  inevi- 
tably and  imminently  fatal." 

The  structural  changes  which  may  take  place  in  the  heart  are:  (1) 
hypertrophy,  which  may  be  physiological  or  pathological ;  (2)  dilatation  of 
one  or  more  of  the  chambers;  (3)  degenerative  changes,  which  may  be 
acute  or  chronic;  (4)  unusual  conditions  such  as  syphilitic  gummata, 
abscess  and  aneurism. 

HYPERTROPHY  OF  THE  HEART 

The  size  of  the  heart  is  proportionate  to  the  body  weight,  and  to  a 
lesser  extent  to  stature.  In  an  adult  man  the  normal  heart  averages  300 
grams  in  weight;  in  an  adult  woman,  250  grams.  As  the  result  of  disease 
the  weight  of  the  heart  may  be  enormously  increased  beyond  these  limits. 

617 


618  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


Fig.   364. — Simple  hypertrophy.      {Jefferson  Medical  College  Museum.) 


Fig.   365. — Hypertrophy  and  dilatation.      {Jefferson  Medical  College  Museum.) 


Fig.   366. — Dilatation.      {Jefferson  Medical  College  Museum.) 


DISEASES    OF    THE    MYOCARDIUM 


619 


Right  pulmon- 
ary artery 


Left  superior 
pulm.  vein 
Left  auricular 
appendix 
Left  inf.  pulm. 
vein 
Left  auricle 


Mitral  valve 
(anterior 
leaflet) 


Fig.    367.— Sagittal  section  of  the  thorax.      Illustrates  how  little  room  for  expansion  there 
is  for  the  heart  between  the  vertebral  column,  and  the  anterior  thoracic  wall. 


620  DISEASES    OF   THE    PERICARDIUM,    HEART,    AND    AORTA 

Instances  have  been  recorded  in  which  the  heart  weighed  1700  and  2500 
grams  respectively.  In  men  the  weight  of  the  heart  to  the  whole  body  is 
about  1  to  170;  in  women  it  is  1  to  183. 

Hypertrophy  may  affect  one  chamber  only,  but  this  is  unusual.  The 
chamber  to  be  first  affected  is  that  one  which  first  is  subjected  to  an  un- 
usual amount  of  work.  Generally  speaking  the  left  ventricle  is  the  cham- 
ber in  which  the  hypertrophy  is  most  marked  even  when  other  portions  of 
the  heart  are  involved  also  (see  Fig.  193). 

Two  forms  of  hypertrophy  are  recognized:  (1)  simple  enlargement, 
without  change  in  the  size  of  the  cavities;  and  (2)  hypertrophy  plus  dila- 
tation of  the  cavities,  sometimes  spoken  of  as  eccentric  enlargement. 
Figs.  364,  365,  and  366  show  very  well  the  change  from  simple  hyper- 
trophy to  dilatation. 


Fig.  368. — A  large  hypertrophied  heart  contrasted  with  one  of  normal  size.      From  a  case 
of  cardiorenal  disease.      {Jefferson  Medical  College  Museum.) 

Formerly  another  form  of  hypertrophy  was  described,  namely,  the 
so-called  concentric  enlargement  of  the  heart.  In  this  state  the  muscle 
is  tremendously  thickened  and  the  cavity  diminished  in  size.  This 
condition  is  now  recognized  as  a  post-mortem  change.  It  is  not  infre- 
quently seen  when  the  autopsy  has  been  held  within  six  hours  of  death 
and  is  due  to  rigor  mortis. 

Hypertrophy  of  the  heart  consists  of  an  increase  in  either  the  number 
or  the  size  of  the  muscle  cells,  or  both.  In  addition  there  is  also  an  increase 
in  the  amount  of  connective  tissue  and  fat.     The  hypertrophied  muscle  is 


DISEASES    OF   THE    MYOCARDIUM  621 

of  a  brownish-red  color  and  the  consistency  is  markedly  increased. 
Slight  degrees  of  hypertrophy  are  not  apt  to  cause  any  disturbance  but 
when  the  enlargement  becomes  excessive  the  mere  size  of  the  organ  may 
produce  cardiac  symptoms.  That  lack  of  space  may  mechanically  inter- 
fere with  the  action  of  the  heart  is  shown  in  Fig.  367.  The  most  extreme 
degrees  of  hypertrophy  are  those  which  occur  as  the  result  of  aortic  re- 
gurgitation, chronic  adherent  pericarditis  and  arterio-sclerosis  and  chronic 
nephritis  (Fig.  368). 

Physiological  Hypertrophy 

At  birth  the  thickness  of  the  walls  of  the  two  ventricles  is  the  same  but 
as  the  left  ventricle  thereafter  assumes  the  chief  burden  of  carrying  on 
the  circulation  it  becomes  physiologically  hypertrophied  to  meet  the 
demand.  Throughout  adult  life  the  heart  possesses  the  ability  to  in- 
crease its  muscular  power  in  exactly  the  same  way  that  the  skeletal 
muscles  respond  to  increased  work  or  exercise.  The  hypertrophy  under 
these  circumstances  is,  however,  rarely  of  the  extreme  degree  that  occurs 
as  the  result  of  pathological  conditions. 

The  normal  heart  may,  therefore,  become  hypertrophied  as  the  result 
of  laborious  occupations  or  as  the  result  of  athletics.  The  effect  of  com- 
petitive athletics  upon  the  heart  has  received  a  great  deal  of  attention 
during  the  past  decade.  So  faf  as  one  can  judge  from  the  literature  on 
the  subject  opinions  as  to  the  hurtfulness  or  harmlessness  of  competitive 
athletics  are  extremely  contradictory.  That  some  hypertrophy  does 
occur  is  unquestioned  but  as  to  whether  the  heart  also  becomes  dilated  or 
whether  it  later  in  life  becomes  more  susceptible  to  endocardial  and 
myocardial  changes  is  still  open  to  question.  In  a  recent  study  of  the 
effect  of  rowing  upon  the  young  adult  heart  Lee,  Dodd  and  Young1 
found  that  there  is  very  little  difference  in  the  size  of  the  heart  of  men  who 
have  been  rowing  for  two  to  four  years,  and  men  who  have  been  rowing 
over  ten  years.  The  hearts  of  these  two  groups  are  very  slightly  larger 
than  the  hearts  of  a  younger  group  who  have  not  as  yet  participated  in 
serious  competitive  rowing.  These  differences  seem  to  be  explained  by 
the  differences  in  age  and  development. 

One  is  probably  safe  in  assuming  that  if  the  heart  is  organically  sound 
excessive  work,  aside  from  causing  slight  physiological  hypertrophy  will 
cause  no  permanent  damage.  It  has  always  seemed  to  me  that  the 
apparent  deleterious  effect  of  athletics  in  later  life  is  to  be  ascribed  to 
changed  habits.  The  man  who  participates  in  athletic  competition,  only 
too  frequently,  upon  leaving  college  ceases  exercising  and  leads  a  sed- 
entary life.  As  a  result  the  cardiac  as  well  as  the  skeletal  muscles,  be- 
come flabby  and  weak. 

Pregnancy  has  been  cited  as  one  of  the  causes  of  physiological  hyper- 
trophy but  enlargement  of  the  heart  in  pregnant  women  is  probably  more 
apparent  than  real.  Owing  to  the  high  position  of  the  diaphragm  in 
pregnancy  the  heart  is  displaced  upward  and  the  area  of  cardiac  dulness 
is  increased  because  the  heart  is  brought  closer  to  the  chest  wall,  and 
also  because  it  lies  more  horizontally. 

Symptoms  and  Signs  of  Physiological  Hypertrophy. — Symptoms  are 
usually  wanting  in  physiological  hypertrophy  except  immediately  after 

1  Boston  Med.  cV-  Surg.  Jour.,  Sept.  30,  1915. 


622  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

severe  exertion.  At  this  time  there  may  be  a  sense  of  throbbing  in  the 
vessels  of  the  neck  and  of  the  heart  itself.  Under  ordinary  conditions 
there  are  no  untoward  symptoms. 

Physical  signs  are  also  trivial  as  the  hypertrophy  is  rarely  as  marked 
as  that  occurring  in  pathological  conditions.  Visible  displacement  of  the 
apex  beat  is  not  conspicuous.  Percussion  usually  shows  some  increase  in 
the  cardiac  dimensions.  On  auscultation  the  first  sound  is  loud  and 
slightly  more  prolonged  than  normal  and  the  second  sound  is  not 
accentuated.  When  the  hypertrophy  is  slight,  such  as  occurs  in  ath- 
letes, the  blood-pressure  is  normal.  Slight  degrees  of  hypertrophy  can 
best?'  be  determined  by  means  of  the  X-rays.  The  examination  is  made 
with  the  patient  standing.  The  X-ray  tube  is  placed  on  a  level  with  the 
mid-portion  of  the  thorax  at  a  distance  of  7  feet  (teleroentgenography) . 

Physiological  hypertrophy  may  be  looked  upon  as  dangerous,  if  the 
heart  is  overacting  when  the  individual  is  at  rest.  Under  the  circum- 
stances the  cardiac  impulse  is  seen  to  be  heaving  or  diffuse,  the  second 
sound  accentuated  and  the  blood-pressure  is  raised. 

Hypertrophy  as  the  Result  of  Disease 

Hypertrophy  may  occur  as  the  result  of  disease  of  the  heart  itself  or 
as  the  result  of  abnormal  conditions  in  -other  portions  of  the  circulatory 
apparatus.  Hypertrophy  under  such  circumstances  is  to  be  looked  upon 
as  a  defensive  action.  In  order  to  overcome  a  valvular  defect  or  the  in- 
creased arterial  resistance  the  heart  hypertrophies  in  proportion  to  the 
increased  amount  of  work  demanded  of  it.  Adami  and  Nicholls  classify 
the  causes  of  hypertrophy  as  follows : 

I.  Obstruction  to  egress  of  blood. 

(a)  Endocardial,  from  stenosis  of  one  of  the  valves. 
(6)  Arterial,  from  diminution  of  the  arterial  lumen,  sclerosis,  con- 
'<■       traction  of  the  smaller  arteries,  etc. 
(c)  Pericardial,  from  complete  synechia. 
II.  Increase  in  the  volume  of  blood  to  be  propelled. 

(a)  Actual  increase  in  the  amount  of  circulating  blood,  plethora, 

Munich  beer  heart,  etc. 
(6)  From  regurgitation,  as  in  mitral  and  aortic  incompetence. 
III.  Increase  in  rate  of  blood  flow. 

(a)  From  tachycardia,  as  in  exophthalmic  goitre. 
(6)  As  a  response  to  systemic  needs,  as  in  the  athlete.     (This  has 
been  considered  under  physiological  hypertrophy.) 

In  practically  all  of  these  conditions  the  hypertrophy  first  manifests 
itself  in  the  left  ventricle  but  as  time  goes  on,  whether  because  of  exces- 
sive work,  or  because  the  exciting  cause  constantly  increases  the  demand 
for  additional  effort,  the  hypertrophy  becomes  general.  The  hyper- 
trophy manifests  itself  first  in  the  right  ventricle  as  the  result  of  fetal  or 
congenital  heart  disease  and  as  the  result  of  certain  pulmonary  affec- 
tions (fibrosis  of  the  lungs,  emphysema,  etc.). 

Valvular  Disease  of  the  Heart.— This  is  by  far  the  commonest  cause 
of  hypertrophy  and  has  been  considered  under  "Chronic  Valvular  Dis- 
ease" (p.  654). 


DISEASES    OF    THE    MYOCARDIUM  623 

Chronic  Adhesive  Pericarditis. — As  the  result  of  adhesions  between 
the  two  layers  of  the  pericardium  and,  often,  with  the  mediastinal  tis- 
sues, the  action  of  the  heart  is  seriously  embarrassed.  The  additional 
work  then  thrown  upon  the  heart  often  leads  to  an  enormous  degree  of 
hypertrophy. 

Arteriosclerosis  and  Chronic  Nephritis. — Next  to  chronic  valvular 
disease  arterio-sclerosis  when  associated  with  chronic  glomerulonephritis 
is  the  most  frequent  cause  of  hypertrophy.  Hypertrophy  arising  under 
these  conditions  has  been  considered  under  chronic  aortitis  or  arterio- 
sclerosis of  the  aorta  (see  Fig.  181). 

" Munich  Beer  Heart." — Excessive  eating  and  drinking  is  a  common 
cause  of  hypertrophy  of  the  heart  and  occurs  with  great  frequency  in 
those  who  consume  large  quantities  of  beer.  A  heart  which  becomes 
enlarged  as  the  result  of  excessive  beer  drinking  has  been  called  the 
"Munich  beer  heart,  "  although  the  condition  is  not  peculiar  to  that  city, 
nor  is  it  confined  exclusively  to  beer.  Excessive  eating  and  drinking 
are  apt  to  be  followed  by  a  temporary  increase  in  the  activity  of  the 
heart,  the  frequency  of  the  pulse  and  the  tension  in  the  arteries.  This 
is  due  to  the  temporary  increase  in  the  specific  gravity  of  the  blood, 
stimulation  of  the  heart  and  blood-vessels  by  the  products  of  metabolism 
and  also  because  the  excessive  ingestion  of  liquids  temporarily  increases 
the  total  amount  of  blood  (Strumpell).  This  so-called  plethoric  condition 
is  usually  seen  in  middle-aged  individuals  who  indulge  freely  in  the 
pleasures  of  the  table  and  lead  a  sedentary  life.  Many  of  the  cases  of 
idiopathic  hypertrophy  properly  belong  under  this  category. 

Tachycardia. — Enlargement  of  the  heart  often  occurs  as  the  result  of 
increased  cardiac  action.  The  most  typical  example  of  this  form  of 
hypertrophy  is  seen  in  Graves'  disease.  In  some  instances  the  rapid 
heart  action  and  the  goitre  may  constitute  the  only  symptoms  of  the 
disease.  Neurotic  individuals  often  suffer  from  tachycardia  and  slight 
cardiac  hypertrophy. 

Symptoms. — Even  extreme  degrees  of  hypertrophy  may  exist  for  a 
long  time  without  producing  symptoms.  This  is  natural  as  the  hyper- 
trophy develops  as  a  defensive  measure  and  for  varying  periods  of  time 
the  circulatory  mechanism  suffers  no  inconvenience.  Eventually,  how- 
ever, the  increased  amount  of  work  tends  to  exhaust  the  muscle  or  the 
demands  on  it  become  so  great  that  compensation  can  no  longer  be 
maintained. 

Premonitory  symptoms  are  usually  present  before  the  heart  becomes 
definitely  insufficient.  Thus  there  may  be  transient  attacks  of  faintness 
or  dizziness,  palpitation,  or  an  annoying  sense  of  fluttering  of  the  heart. 
Shortness  of  breath  or  a  sense  of  precordial  oppression  is  common,  espe- 
cially after  exertion.  In  some  instances  the  violent  action  of  the  heart 
may  give  rise  to  pain  in  the  region  of  the  heart,  throbbing  sensations  in 
the  head  and  neck  and  to  pulsatile  noises  in  the  ears.  Finally,  dilata- 
tion supervenes  and  the  symptoms  and  physical  signs  of  failing  com- 
pensation appear.  These  differ  in  no  particular  from  those  occurring 
in  chronic  valvular  disease. 

Physical  Signs. — Inspection. — The  apex  beat  is  displaced  downward 
and  outward.  It  may  be  but  slightly  removed  from  its  normal  position, 
or,  as  in  the  case  of  marked  hypertrophy,  it  may  be  in  the  sixth  or  seventh 
interspace  and  as  far  to  the  left  as  the  mid-axillary  line.     The  cardiac 


624  DISEASES    OF    THE    PERICARDIUM;    HEART,    AND    AORTA 

impulse  is  seen  as  a  gentle  heave.  In  very  thick-chested  individuals 
neither  the  apex  beat  nor  the  heaving  impulse  may  be  visible,  even  when 
a  considerable  degree  of  hypertrophy  is  seen. 

Palpation. — This  serves  to  confirm  the  location  of  the  apex  beat  and 
also  the  rather  diffuse  and  heaving  character  of  the  impulse.  By  pal- 
pation the  amount  of  hypertrophy  can  be  roughly  estimated  by  the 
strength  of  the  impulse.  The  cardiac  impulse  is  not  only  felt  to  be 
forcible  and  diffuse  but  in  addition  the  overlying  ribs  may  be  distinctly 
lifted.  The  forcibleness  of  the  impulse  is  sometimes  better  appreciated 
by  pressing  the  fingers  into  the  intercostal  spaces. 

In  those  cases  in  which  the  hypertrophy  is  due  in  large  part  to  high 
arterial  tension  (chronic  nephritis,  lead  poisoning,  gout,  etc.)  the  pulse 
will  feel  full  and  tense.  It  usually  takes  considerable  pressure  to  com- 
pletely obliterate  the  pulse.  In  such  cases  the  blood-pressure  is  alwajrs 
high. 

Percussion. — Unless  the  hypertrophy  is  very  slight  the  area  of  cardiac 
dulness  will  be  found  to  be  increased  downward  and  to  the  left.  Dulness 
to  the  right  of  the  sternum  is  also  increased  due  to  the  dilatation  and 
hypertrophy  of  the  right  ventricle. 

Auscultation.- — Unless  the  hypertrophy  is  due  to  chronic  valvular 
disease  or  slight  dilatation  is  also  present,  no  murmurs  are  heard.  The 
first  sound  is  loud,  low-pitched  and  more  prolonged  than  normal  and  gives 
the  impression  of  a  powerfully  contracting  muscle.  The  second  sound  is 
usually  very  distinct  at  the  apex.  At  the  aortic  area  the  second  sound 
may  be  accentuated  and  ringing  in  character.  In  such  cases  there  is 
usually  present  a  chronic  aortitis.  Reduplication  of  the  first  sound  at  the 
apex  may  be  the  first  intimation  of  oncoming  dilatation  of  the  left 
ventricle. 

DILATATION  OF  THE  HEART 

Just  as  in  the  case  of  hypertrophy  one  or  all  of  the  chambers  of  the 
heart  may  be  involved.  In  mitral  stenosis,  for  instance,  distention  of  the 
left  auricle  may,  for  a  time,  be  the  only  evidence  of  dilatation.  As  the 
back  pressure  becomes  greater  and  greater  the  right  ventricle  also  be- 
comes dilated  as  does  also  finally  the  right  auricle.  Generally  speaking, 
the  use  of  the  term  ''dilatation  of  the  heart"  has  reference  to  dilatation 
of  the  left  ventricle,  although,  as  a  rule,  the  right  ventricle  is  also  dilated. 

An  increase  in  the  capacity  of  one  or  more  of  the  chambers  of  the 
heart  may  be  clue  to  temporary  distention  or  to  permanent  dilatation. 
By  the  term  distention  we  have  in  mind  a  condition  in  which  the  chamber 
enlarges  temporarily  as  the  result  of  some  unusual  physiological  demand, 
and  when  this  requirement  has  ceased  the  normal  condition  returns. 
Thus  in  cases  of  relative  tricuspid  insufficiency  the  right  ventricle  may 
become  distended  temporarily  as  the  result  of  exertion  necessitating 
great  muscular  and  intrathoracic  straining.  In  such  cases  the  valvular 
orifice  is  stretched  as  the  result  of  the  distention  of  the  ventricle  and  a 
leakage  occurs.  In  like  manner  the  enlargement  of  the  left  ventricle  in 
compensated  valvular  disease  is  to  be  regarded  as  a  physiological  disten- 
tion and  not  a  dilatation,  even  if  the  condition  is  permanent  and  not 
temporary.  The  distention  is  caused  by  the  increased  volume  of  blood 
the  left  ventricle  is  forced  to  handle.  In  the  great  majority  of  cases 
hypertrophy  quickly  takes  place  in  order  to  meet  the  increased  work. 


DISEASES    OF   THE    MYOCARDIUM  625 

When,  however,  the  heart  muscle  no  longer  responds  to  this  demand  for 
increased  work,  the  ventricle  then  becomes  pathologicallv  distended  or 
dilated  (Fig.  366). 

Dilatation  is  seen  in  the  most  characteristic  aspects  when  the  heart 
muscle  is  the  seat  of  degenerative  changes.  Thus  as  the  result  of  fatty  or 
fibroid  degeneration  the  muscle  becomes  weak,  inefficient  and  unable  to 
meet  the  normal  demands.  Inability  of  the  ventricle  to  properly  empty 
itself  quickly  leads  to  dilatation. 

That  an  anatomical  defect  is  not  the  sole  cause  of  dilatation  is  evident 
from  the  fact  that  hearts  are  seen  at  the  autopsy  table  in  which  marked 
degenerative  changes  have  taken  place  and  yet  these  hearts  during  life 
have  performed  their  work  fairly  satisfactorily  and  without  becoming 
dilated.  Mackenzie  believes  that  the  loss  of  muscular  tonicity  is  the 
essential  feature  of  dilatation.  So  long  as  the  tonicity  remains  unim- 
paired, or  is  only  slightly  diminished,  dilatation  does  not  occur  even  when 
there  is  present  a  serious  anatomical  lesion.  When,  however,  the  tonicity 
is  lost  either  as  the  result  of  the  exhaustion  of  a  hypertrophied  muscle  or 
because  of  disease,  the  heart  dilates. 

This  has  been  demonstrated  experimentally.  Thus  if  extra  work  is 
suddenly  demanded  of  the  left  ventricle  as  the  result  of  clamping  the  aorta, 
the  chamber  dilates  (physiologically  distends)  and  the  systolic  output  is 
diminished.  In  healthy  hearts  there  occurs,  as  the  result  of  increased 
tonicity,  an  increase  in  the  systolic  output  and  the  ventricle  empties  itself 
properly.  If,  however,  the  obstruction  is  too  great  or  the  muscle  is  in- 
capable of  responding,  the  ventricle  becomes  pathologically  dilated 
(Frank,  Hirschf elder). 

Dilatation,  therefore,  may  be  defined  as  a  condition  in  which  as  the 
result  of  loss  of  muscle  tone,  a  diseased  heart  muscle  or  one  which  finally 
exhausts  its  reserve  power  is  no  longer  able  to  carry  on  the  extra  work 
demanded  of  it. 

Dilatation  of  the  heart  may  be  acute  or  chronic.  Acute  dilatation 
may  occur  as  the  result  of  excessive  muscular  exertion,  especially  in  in- 
dividuals out  of  training  or  as  the  result  of  toxic  processes,  such  as  diph- 
theria, typhoid  fever  or  pneumonia.  Sudden  mental  shock  also  may 
lead  to  an  acute  dilatation  of  the  heart. 

Chronic  dilatation  is  often  associated  with  or  is  the  sequel  of  hyper- 
trophy. It  usually  occurs  as  the  result  of  inadequate  nutrition  and  in- 
creased endocardial  pressure  and  to  an  increased  demand  for  hypertrophy. 

Degenerative  changes  in  the  heart  muscle  are  very  commonly  associated 
with  dilatation.  At  the  autopsy  table  the  dilated  heart  is  found  to  be 
much  enlarged  and  distended  with  blood.  The  walls  are  thin,  flabby, 
softer  than  normal  and  often  pale  in  color  from  fatty  changes.  Because  of 
thinness  of  the  wall  of  the  right  ventricle  this  chamber  usually  shows  the 
most  marked  evidence  of  dilatation.  The  auriculo-ventricular  orifices 
ace  widely  dilated  and  the  septa  may  bulge  toward  the  less  affected  side. 

Symptoms  and  Physical  Signs  of  Dilatation. — The  symptoms  of  car- 
diac dilatation  vary  greatly.  They  may  consist  of  nothing  more  than 
slight  dyspnea  and  a  sense  of  precordial  oppression  after  exertion.  If, 
however,  the  ventricle  habitually  fails  to  expel  all  of  its  contents,  the 
symptoms  become  more  and  more  marked  and  the  failure  of  the  circula- 
tion manifests  itself  in  distant  organs  and  tissues.  The  subcutaneous 
tissues  become  edematous,  the  lungs  congested,  effusions  take  place  in  the 

40 


626  DISEASES    OP   THE    PERICARDIUM,    HEART,    AND    AORTA 

serous  cavities  and  the  liver  becomes  engorged.  The  urine  is  scanty  in 
amount,  of  a  high  specific  gravity  and  contains  much  albumen. 

Often  there  will  be  present  reflex  sensory  symptoms  as  shown  by  areas 
of  hyperalgesia  of  the  skin  and  muscles  of  the  left  chest,  axillary  fold  and 
the  sternomastoid  and  trapezius  muscles  (Mackenzie)  (see  p.  43). 

The  physical  signs  of  dilatation  are  as  follows :  Displacement  of  the 
apex  beat  downward  and  outward;  diffuse  pulsation;  the  evidences  of 
general  venous  engorgement;  marked  increase  of  cardiac  dulness  in  the 
transverse  diameter ;  the  presence  of  murmurs  of  relative  insufficiency  at 
the  mitral  and  tricuspid  areas;  and  loss  of  the  muscular  quality  of  the 
first  sound. 

The  subject  of  failing  compensation  is  considered  more  in  detail  under 
the  heading  chronic  valvular  disease. 

MYOCARDITIS 

The  term  myocarditis  is  not  altogether  a  satisfactory  one.  It  is 
retained  because,  by  common  usage,  it  implies  disease  of  the  myocardium. 
Strictly  speaking  myocarditis  is  a  misnomer  inasmuch  as  many  of  the 
conditions  embraced  under  the  term,  are  of  a  degenerative  rather  than 
of  an  inflammatory  nature.  These  changes  impair  the  structure  and 
functional  activity  of  the  cardiac  muscle,  and  may  affect  all  or  only  a 
portion  of  the  myocardium.  In  many  instances  the  ganglia  and  nerves 
of  the  heart  are  also  involved.  The  severity  of  the  lesion  will  depend  in 
some  cases,  on  its  extent  and  in  others,  on  its  location.  The  location  is 
an  extremely  important  factor  for  if  the  muscle  fibers  composing  the  car- 
diac conduction  path  (auriculo-ventricular  bundle)  are  diseased,  the 
results  are  much  more  serious  than  if  an  equal  amount  of  non-specialized 
tissue  is  implicated.  It  is  important  to  bear  this  fact  in  mind  as  there 
are  many  cases  which  during  life  present  marked  symptoms  of  cardiac  in- 
sufficiency and  yet  at  the  autopsy  no  evidence  of  myocarditis  is  found. 
The  true  explanation  of  this  discrepancy  probably  lies  in  the  fact  that  a 
routine  autopsy  is  apt  to  overlook  these  small  specialized  areas  which  may 
be  the  only  portion  of  the  myocardium  involved.  Disease  of  the  auriculo- 
ventricular  bundle  (bundle  of  His)  possesses  a  pathology  of  its  own  and 
will  be  considered  separately  (pp.  169  and  187). 

Myocarditis  may  occur  in  an  acute  and  in  a  chronic  form. 

Acute  Myocarditis 

Etiology. — With  few  exceptions  acute  myocarditis  occurs  as  the  result 
of  some  acute  infectious  process.  Involvement  of  the  myocardium  is  so 
frequent  in  certain  of  the  acute  infections  that  the  possibility  of  its 
presence  should  always  be  borne  in  mind. 

Acute  rheumatic  fever  is  one  of  the  most  important  of  the  acute  infections 
in  this  regard.  It  is  not  sufficiently  appreciated  that  in  most  cases  of 
rheumatic  endocarditis  the  myocardium  is  also  involved,  and  it  is  to  the 
latter  that  many  cases  of  cardiac  hypertrophy  and  chronic  myocarditis 
owe  their  origin.  Coombs1  has  pointed  out  that  death  in  the  rheumatic 
carditis  of  childhood  is  generally  directly  due  to  the  myocardial  lesions. 

Diphtheria. — It  is  well  known  that  in  diphtheria  serious  myocardial 

1  Quarterly  Jour.  Med.,  October,  1908. 


DISEASES    OF    THE   MYOCARDIUM  627 

changes  are  often  present  and  that  sudden  death  is  not  an  infrequent 
occurrence.  The  slightest  evidence  of  cardiac  weakness  or  irregularity, 
other  than  sinus  arrhythmia,  during  or  immediately  after  an  attack  of 
diphtheria  is  to  be  looked  upon  as  serious.  In  such  cases  every  precaution 
should  be  taken  to  avoid  even  the  most  trifling  exertion. 

Influenza  is  often  associated  with  marked  myocardial  changes.  It  is 
important  to  remember  that  the  evidences  of  cardiac  mischief  usually 
appear  some  time  after  the  disappearance  of  the  primary  disease.  In  the 
aged  or  in  the  debilitated,  sudden  death  from  cardiac  failure,  several 
weeks  after  apparent  recovery  from  influenza,  is  not  an  unusual  accident. 

Syphilis. — It  is  now  recognized  that  myocardial  changes  may  occur  in 
the  early  stages  of  syphilis  (see  " Myocardial  Changes  Due  to  Syphilis"). 

Typhoid  f eve?'  is  quite  constantly  associated  with  myocardial  changes. 
Although  sudden  death,  due  to  cardiac  failure,  is  rare  in  typhoid  fever, 
the  heart  is  often  permanently  damaged  to  a  greater  or  lesser  extent. 
Acute  myocarditis  may  occur  also  in  scarlatina,  smallpox  and  gonorrhea. 

Sudden  blocking  of  one  of  the  coronary  vessels  by  an  embolism  or 
thrombus  is  a  not  infrequent  cause  of  localized  acute  myocarditis.  The 
sudden  shutting  off  of  the  blood  supply  leads  to  a  very  rapid  degenera- 
tion or  acute  necrosis  in  the  affected  area.  If  the  embolus  is  septic  in 
origin-  an  abscess  results.  Acute  abscess  formation  in  the  myocardium 
may  be  part  of  a  general  pyemic  process  such  as  occurs  in  puerperal  fever 
or  malignant  endocarditis.  Among  9940  autopsy  records  analyzed  by 
Norris  there  were  6  cases  of  acute  suppurative  myocarditis. 

Morbid  Anatomy. — The  pathological  picture  of  acute  myocarditis 
will  depend  on  the  exciting  cause.  The  most  frequent  of  the  myocardial 
changes  is  an  acute  parenchymatous  degeneration  which  results  from  the 
action  of  toxins  in  the  course  of  the  acute  infections.  It  is  a  diffuse 
process  and  varies  greatly  in  severity.  It  may  consist  of  nothing  more 
than  a  slight  cloudy  swelling.  In  well-marked  cases  there  is  in  addi- 
tion a  granular  degeneration  of  the  muscle  fibers.  The  myocardium 
then  presents  a  pale  turbid  or  opaque  appearance  which  has  been  likened, 
by  Adami,  to  parboiled  meat  or  raw  fish.  The  muscle  is  soft,  flabby  and 
readily  torn.  The  ventricles,  especially  the  left,  are  usually  dilated. 
Microscopically  the  muscle  fibers  are  seen  to  be  swollen,  fragmented  and 
the  striations  more  or  less  obscured  by  minute  granules  which  are  prob- 
ably albuminoid  in  nature. 

Less  frequently  an  acute  interstitial  myocarditis  occurs  as  the  result 
of  one  of  the  acute  infections  or  acute  pericarditis.  In  this  form  there 
are  collections  of  inflammatory  leukocytes  between  the  muscle  fibers 
and  connective-tissue  proliferation.  Minute  hemorrhagic  areas  are  often 
present  also. 

When  the  change  has  been  slight  in  degree,  recovery  of  the  muscle  is 
usually  complete.  In  other  instances  the  damage  is  so  great  that  death 
ensues  as  the  result  of  cardiac  failure;  in  still  other  instances  the  muscle 
remains  permanently  impaired  and  a  chronic  myocarditis  eventually 
develops. 

When  the  nutrition  of  the  heart  is  interfered  with  as  the  result  of  the 
sudden  blocking  of  one  of  the  branches  of  the  coronary  artery  a  localized 
myocarditis  occurs.  This  may  be  septic  or  benign  in  character.  The 
former  is  encountered  in  cases  of  general  sepsis  in  which  the  finer  branches 
of  the  coronary  artery  are  blocked  with  septic  emboli.     As  a  result  small 


628  DISEASES    OF   THE    PERICARDIUM,    HEAET,    AND    AORTA 

abscesses  develop  in  the  myocardium.  These  vary  in  size  from  a  pin- 
head  to  a  split  pea. 

The  benign  form  may  occur  as  the  result  of  an  embolism  or  thrombosis 
in  a  coronary  artery,  the  seat  of  atheromatous  changes.  In  such  cases 
the  blood  supply  to  a  given  area  of  the  myocardium  is  suddenly  shut 
off.  It  is  variously  designated  anemic  necrosis,  acute  softening  and 
myomalacia  cordis.  Cardiac  infarcts  are  most  commonly  seen  in  the 
left  ventricle  and  septum  which  are  supplied  by  the  anterior  coronary 
artery.  The  appearance  of  the  infarct  depends  on  its  age.  The  changes 
which  .follow  blocking  of  one  of  the  branches  of  the  coronary  artery  are 
usually  rapid.  At  first  the  affected  area  is  yellow  or  grayish-red  in  color. 
It  is  of  an  irregular  or  wedge  shape  and  projects  slightly  above  the  sur- 
face. The  initial  change  is  a  coagulative  necrosis  and  softening.  The 
weakened  point  in  the  heart  wall  may  rupture  and  cause  sudden  death. 
This  is  rare.  The  usual  termination  is  the  transformation  of  the  infarct 
into  scar  tissue. 

Symptoms. — It  too  often  happens  that  the  physician  in  his  anxiety 
over  the  symptoms  due  to  the  primary  disease  loses  sight  of  the  secondary 
changes  which  may  occur.  At  the  best,  the  initial  symptoms  indica- 
tive of  myocardial  weakness  in  the  acute  infections  are  slight,  easily 
overlooked  and  may  be  entirely  absent.  The  sudden  death  of  the  patient 
may  be  the  first  intimation  that  cardiac  weakness  has  been  present.  In 
some  instances  the  myocardial  weakness  manifests  itself  during  the 
febrile  stage;  in  others,  notably  influenza  and  diphtheria,  circulatory 
disturbances  may  not  appear  until  much  later. 

The  symptoms  of  myocardial  weakness  are  restlessness  or  apathy, 
breathlessness  on  exertion,  a  sense  of  constriction  in  the  chest  and,  at 
times,  pain  which  is  anginoid  in  character.  In  the  more  serious  cases 
there  will  be  evidences  of  dilatation  of  the  heart,  namely,  cyanosis, 
dyspnea,  precordial  and  hepatic  pain,  vomiting  and  edema. 

Physical  Signs. — Inspection. — In  the  severe  cases  the  patient  often 
presents  a  pallid  appearance  and  is  either  apathetic  or  very  restless.  If 
dilatation  has  occurred  there  may  be  cyanosis  and  more  or  less  edema  of 
the  lower  extremities.  Inspection  of  the  precordium  may  be  negative 
but  if  considerable  dilatation  has  taken  place  the  apex  beat  is  displaced 
to  the  left  and  the  impulse  may  be  diffuse. 

Palpation. — This  serves  to  locate  the  apex  beat  and  to  determine  the 
force  of  the  impulse.  Of  more  importance  is  the  character  of  the  pulse. 
The  most  common  change  in  the  pulse  is  feebleness  with  or  without  an 
increase  in  the  rate.  Much  less  frequently  there  is  a  bradycardia.  Un- 
due slowness  of  the  pulse  is  most  often  encountered  some  weeks  after 
recovery  from  an  attack  of  influenza.  The  bradycardia  may  be  vagal 
in  origin  or  it  may  be  caused  by  changes  in  the  auriculo-ventricular  bundle. 
The  most  serious  change  to  be  noted  in  the  pulse  is  lability  and  arrhyth- 
mia. The  latter  may  be  due  to  changes  in  the  force  of  the  respective 
beats  or  to  alterations  in  the  rhythm.  The  blood-pressure  in  acute 
myocarditis  is  usually  low. 

Percussion. — Unless  considerable  dilatation  is  present  there  will  be 
no  change  noted.  An  increase  in  the  transverse  diameter  of  the  heart 
speaks  for  dilatation. 

Auscultation.- — If  the  myocardial  weakness  is  at  all  marked  the  heart 
sounds  are  accentuated  and  short  and  the  first  sound  lacks  the  normal 


DISEASES    OF    THE    MYOCARDIUM  629 

muscular  quality.  The  second  pulmonic  sound  is  usually  sharply  accen- 
tuated. Either  the  first  or  second  sound  may  be  reduplicated;  if  redupli- 
cation of  the  former  occurs  it  may  be  the  first  intimation  of  dilatation.  A 
functional  murmur  at  the  mitral  area  is  common  and  in  some  instances  a 
similar  murmur  may  be  heard  also  at  the  tricuspid  area. 

Diagnosis. — As  has  been  pointed  out,  the  diagnosis  of  acute  myo- 
carditis is  not  easy  and  in  many  instances  is  a  matter  of  conjecture. 
Armed  with  the  knowledge  that  the  condition  is  a  frequent  accompani- 
ment of  the  acute  infections,  the  physician  should  always  be  alert  to  detect 
the  slightest  alterations  in  the  circulatory  mechanism.  No  matter  how 
trivial  these  may  appear,  they  should  be  given  serious  consideration  and 
measures  taken  to  guard  the  patient  against  undue  exertion.  It  is  im- 
portant to  bear  in  mind  that  the  evidences  of  myocardial  weakness  may 
not  appear  until  several  weeks  after  the  patient  has  recovered  from  the 
acute  infection.  For  this  reason  patients  who  have  recovered  from  in- 
fluenza and  diphtheria,  especially  the  latter,  should  be  kept  under 
supervision. 

Chronic  Myocarditis 

Etiology. — The  causes  of  chronic  myocarditis  are  extremely  varied. 
In  every  instance  the  chronic  lesion  is  the  sequel  of  .an  acute  process  but 
in  the  great  majority  of  instances  the  latter  passes  unrecognized.  As  a 
rule  the  progress  of  the  myocardial  change  from  an  acute  inflammatory 
or  degenerative  process  to  one  of  a  chronic  nature  is  insidious  and  gives 
no  evidence  of  its  presence  until  more  or  less  serious  muscular  insufficiency 
develops.  Not  infrequently  urgent  cardiac  symptoms  develop  suddenly 
and  in  the  midst  of  apparent  health.  If  this  occurs  in  relatively  young 
or  middle-aged  individuals  syphilis  is  to  be  suspected. 

One  of  the  most  important  causes  of  chronic  myocardial  changes  is 
disturbance  of  the  coronary  circulation  which  results  in  poor  cardiac 
nutrition.  This  may  be  abrupt  as  the  result  of  an  embolus  or  thrombus 
in  which  case  a  coagulative  necrosis  takes  place  and  later  scar  tissue  is 
formed.  More  commonly  the  nutrition  of  the  heart  muscle  is  lowered 
by  reason  of  sclerosis  of  the  coronary  vessels.  The  extent  of  the  myo- 
cardial changes  will  depend  on  the  amount  of  vascular  damage.  The 
causes  of  the  coronary  sclerosis  are  the  same  as  those  producing  arterio- 
sclerosis elsewhere.  The  blood  supply  to  the  heart  may  be  seriously  inter- 
fered with  by  closure  of  the  mouths  of  the  coronary  vessels  as  the  result 
of  disease  of  the  first  part  of  the  aorta,  the  coronary  vessels  themselves 
being  healthy.  This  is  especially  apt  to  occur  as  the  result  of  syphilitic 
aortitis. 

It?  is  well  known  that  the  final  stage  in  chronic  valvular  disease  is,  in 
the  great  majority  of  instances,  muscular  insufficiency  due  to  myocardial 
degeneration.  This  is  brought  about  partly  by  increased  work  and  partly 
by  perversions  in  cardiac  metabolism.  Similarly  the  hypertrophy  and 
dilatation  which  result  from  persistent  cardiac  strain  whether  due  .to 
physical  exertion,  to  hypertension  in  the  arteries  or  to  adherent  pericardi- 
tis, lead  to  myocardial  degeneration  because  of  the  increased  work  de- 
manded of  the  heart.  There  may  be  included  in  this  group  also  those 
instances  in  which  the  heart  for  long  periods  of  time  beats  at  a  greatly 
increased  rate,  the  most  notable  example  of  which  is  seen  in  exophthalmic 
goitre. 


630  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

Myocarditis  has  also  been  attributed  to  high-pressure  methods  of 
living,  severe  physical  labor  and  hardship  and  the  chronic  infections,  espe- 
cially syphilis.  Inasmuch  as  these  factors  are  very  frequently  the  under- 
lying causes  of  general  arterio-sclerosis  it  is  probable  that  sclerosis  of  the 
coronary  vessels  is  the  actual  cause  of  the  myocardial  changes. 

Finally  degenerative  changes  may  be  brought  about  by  chronic  in- 
toxications, such  as  perversions  of  metabolism,  alcoholism,  nicotine 
poisoning,  phosphorus  poisoning,  the  prolonged  use  of  arsenic,  etc. 

The  muscular  insufficiency  usually  manifests  itself  first  in  that  portion 
of  the  heart  in  which  the  strain  has  been  greatest.  Thus  in  general  arterio- 
sclerosis, aortic  insufficiency,  and  the  hypertrophy  due  to  excessive  exer- 
tion, it  is  the  left  ventricle  which  is  subjected  to  the  greatest  strain.  On 
the  other  hand,  chronic  pulmonary  lesions,  such  as  emphysema,  asthma 
or  fibrosis  of  the  lungs  and  mitral  lesions,  throw  the  greatest  amount  of 
work  on  the  right  ventricle  and  in  such  cases  it  is  this  chamber  which  is 
the  first  to  become  embarrassed. 

Morbid  Anatomy. — The  most  common  anatomical  lesions  are  fibroid 
or  fatty  changes. 

Fibrous  myocarditis  or  fibroid  degeneration  may  be  limited  to  a  small 
localized  area  or  there  may  be  numerous  small  patches  of  fibrosis  or  the 
change  may  be  diffuse  in  character.  The  localized  patch  following  an 
infarct  from  blocking  of  one  of  the  coronary  vessels  has  been  referred 
under  acute  myocarditis.  The  patchy  and  diffuse  forms  are  most  fre- 
quently due  to  sclerosis  of  the  coronary  arteries.  In  some  cases  numerous 
small  areas  of  anemic  necrosis  undergo  fibroid  changes;  in  others,  the  inter- 
ference with  the  blood  supply  causes  a  slow  and  gradual  fibroid  degenera- 
tion. Fibroid  areas  may  result  also  from  areas  of  acute  inflammation 
or  as  the  result  of  the  action  of  a  toxin. 

The  fibrosis  is  found  most  often  in  the  apex  of  the  left  ventricle  and 
in  the  septum  (Fig.  369).  It  may  be  limited,  however,  to  the  papillary 
muscles,  the  right  ventricle,  or  the  auricles.  Aneurism  of  the  heart  wall 
always  has  its  origin  at  the  site  of  a  fibroid  area.  Rupture  of  the  heart 
is  an  occasional  accident  resulting  from  chronic  fibrous  myocarditis. 

Fatty  Heart. — This  is  a  relatively  common  condition.  Two  forms  are 
recognized,  namely  fatty  degeneration  and  fatty  infiltration  or  fatty 
overgrowth. 

Fatty  degeneration  is  met  with  in  cachectic  conditions,  in  prolonged 
infections,  and  as  an  accompaniment  of  or  sequel  of  acute  parenchymatous 
degeneration.  The  condition  often  occurs  in  an  extreme  form  in  perni- 
cious anemia  and  phosphorus  poisoning.  Disease  of  the  coronaries  may 
cause  fatty  degeneration  although  fibroid  changes  more  frequently  result. 

The  heart  muscle  is  pale  in  color,  and  soft  in  consistency,  so  that  the 
finger  readily  penetrates  it.  The  heart  maj^  be  so  softened  and  so  flabby 
that  it  entirely  loses  its  normal  contour  when  removed  from  the  bod}r. 
Very  commonly  the  muscle  will  show  streaks  or  patches  of  yellowish- 
brown,  the  so-called  "tabby  cat"  striation.  The  striations  are  usually 
well  marked  in  the  papillary  muscles. 

Fatty  degeneration  is  usually  most  apparent  in  the  left  ventricle,  near 
the  apex.  The  right  ventricle,  the  septum  and  auricles  are  involved  in 
the  order  mentioned. 

Microscopically  tiny  globules  of  fat  are  seen  deposited  in  the  muscle 
fibers  and  not  between  them. 


Fig.   369. — Old    soars    in    the    heart-wall   (chronic  fibrous    myocarditis).      (MacCallum, 
"Text-Book  of  Pathology.") 


DISEASES    OF    THE    MYOCARDIUM  631 

Fatty  infiltration  or  fatty  overgrowth  is  a  condition  in  which  the  heart  is 
encased  in  a  thick  layer  of  fat.  In  extreme  cases  the  muscle  may  be 
completely  hidden.  In  addition  fat  is  deposited  between  but  not  in  the 
muscle  fibers.  Usually  fatty  infiltration  is  a  part  of  general  obesity  but 
it  occasionally  is  met  with  in  the  absence  of  undue  stoutness. 

Brown  atrophy  is  a  common  condition  and  is  usually  found  in  associa- 
tion with  valvular  lesions  and  in  senile  hearts.  The  color  of  the  heart 
muscle  is  reddish-brown  and  the  consistency  is  much  increased. 

Of  the  more  unusual  anatomical  lesions  may  be  mentioned  fragmenta- 
tion and  segmentation  of  the  muscle  fibers,  calcareous  degeneration, 
amyloid  degeneration  and  hyaline  transformation. 

Symptoms. — The  clinical  picture  of  chronic  myocarditis  is  a  varied 
one.  Not  infrequently  symptoms  are  absent  or  very  trivial  in  character 
and  yet  well-marked  lesions  are  found  at  the  autopsy.  Sudden  death  may 
be  the  first  intimation  that  a  serious  cardiac  lesion  is  present.  On  the 
other  hand,  the  clinical  picture  may  point  clearly  to  insufficiency  of  the 
heart  muscle  and  yet  at  the  autopsy  no  lesion  is  found.  Cabot  in  a  com- 
parison of  the  clinical  and  pathological  diagnoses  of  myocarditis  found 
that  the  condition  was  correctly  recognized  in  22  per  cent.,  overlooked 
in  26  per  cent.,  and  diagnosticated  when  not  present  in  52  per  cent.  Of 
the  last-mentioned  group  it  may  be  said  that  small  localized  areas  of  dis- 
ease, particularly  in  the  specialized  tissue  of  the  conduction  path,  may 
have  escaped  notice.  Careful  microscopic  studies  are  much  needed  in 
that  group  of  cases  which  give  symptoms  of  cardiac  insufficiency  but 
which  at  death  show  no  gross  anatomical  lesion. 

Unless  symptoms  are  entirely  wanting  the  one  outstanding  feature 
of  chronic  myocardial  degeneration  is  cardiac  insufficiency.  To  a  greater 
or  lesser  extent  the  symptoms  which  characterize  this  condition  will 
always  be  present.  Very  often,  however,  the  symptoms  of  cardiac  weak- 
ness are  overshadowed  by  some  special  symptom  complex,  as  for  instance, 
angina  pectoris,  Stokes-Adams  disease,  or  hypertension  with  or  without 
chronic  nephritis. 

The  first  intimation  of  myocardial  weakness  may  be  transient  attacks 
of  dizziness  or  faintness  and  this  is  especially  apt  to  occur  in  robust, 
middle-aged  men  with  arterio-sclerosis.  Breathlessness  and  a  sense  of 
oppression  in  the  chest  after  some  slight  but  unusual  exertion  are  early 
symptoms.  Pain  is  especially  apt  to  occur  if  the  exertion  follows  a  meal. 
The  pain  passes  off  with  the  eructation  of  gas.  In  such  cases  the  trouble 
may  be  attributed,  erroneously,  to  dyspepsia.  Slight  swelling  of  the 
feet  and  ankles  may  be  an  early  manifestation.  Associated  with  the 
dyspnea  there  may  be  anginoid  attacks  of  pain  and  as  has  been  stated, 
true  angina  may  dominate  the  picture.  In  other  instances,  the  patient 
suffers  from  collapse  in  which  he  sweats  and  has  a  feeble  but  slow  pulse. 

The  symptoms  just  given  may  be  transient  but,  as  a  rule,  they  tend  to 
become  increasingly  severe  until  the  characteristic  picture  of  dilatation 
or  incompetence  appears.  The  dyspnea  persists,  even  at  rest,  and 
Cheyne-Stokes  breathing  may  occur.  Cough  is  often  annoying  and  the 
sputum  hemorrhagic  as  the  result  of  pulmonary  infarcts.  The  patient 
is  pale,  usually  cyanosed  and  there  is  often  edema  of  the  lower  extremities. 
Owing  to  the  back  pressure  in  the  veins  the  liver  becomes  engorged  and 
painful  and  in  addition  there  is  nausea  and  vomiting.  In  the  terminal 
stages  mental  symptoms  are  common. 


632  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

In  obese  individuals  with  fatty  overgrowth  of  the  heart,  dyspneic 
attacks,  resembling  asthma,  are  common.  The  puffing  respiration  of 
such  individuals  is  usually  ascribed  to  their  obesity  but  more  often  it  is  an 
evidence  of  cardiac  weakness.  In  some  individuals,  dyspnea  without 
cyanosis  results  from  acidosis,  probably  due  to  insufficient  renal  elimina- 
tion. When  acidosis  as  indicated  by  the  alveolar  carbon  dioxid  tension, 
occurs  in  cardiac  and  cardio-renal  disease,  it  is  associated  with  an  in- 
creased stimulability  to  carbon  clioxicl  in  the  inspired  air.  In  addition, 
these  patients  are  subject  to  attacks  of  bronchitis,  and  to  attacks  of 
dizziness  and  faintness.  In  some  corpulent  individuals  the  face  has  a 
dusky,  congested  appearance  which  is  commonly  ascribed  to  ruddy  health 
but  which  in  reality  is  an  evidence  of  venous  stasis. 

Physical  Signs. — In  taking  up  the  physical  signs  of  myocarditis  no 
mention  will  be  made  of  the  secondary  changes  which  take  place  in  the 
heart  as  the  result  of  hypertrophy  whether  due  to  valvular  lesions  or  to 
hypertension.  These  have  been  considered  under  their  appropriate 
headings.  The  signs  described  here  are  those  which  occur  in  association 
with  fibrosis  of  the  heart  muscle  and  in  the  so-called  fatty  heart. 

Inspection. — The  apex  beat  may  be  seen  in  its  normal  position,  but  as 
a  rule,  it  is  displaced  to  a  greater  or  lesser  distance  beyond  the  nipple  line 
and  the  impulse  is  feeble  and  diffuse.  Pulsation  of  the  -vessels  in  the 
neck  may  be  marked. 

Palpation. — The  pulse  shows  the  greatest  variations.  It  may  be 
irregular,  either  as  to  force  or  rhythm,  and  rapid  or  slow.  In  many  cases 
it  is  simply  weak.  Irregularity  is  perhaps  the  most  common  abnormality 
but  is  often  not  present  until  the  late  stages  of  the  disease.  The  arrhyth- 
mia may  be  due  to  extrasystoles  or  to  auricular  fibrillation.  A  very  slow 
pulse  is  not  infrequent  and  often  there  are  associated  with  it  other 
symptoms  characteristic  of  the  Stokes-Adams  syndrome.  Slight  physical 
exertion  markedly  accelerates  the  pulse  rate  which  remains  high  for  some 
time  afterward. 

The  blood-pressure  varies  according  to  the  underlying  cause  of  the 
myocarditis.  In  fatty  degeneration  it  is  often  low  but  in  spite  of  well- 
marked  cardiac  lesions  the  normal  pressure  may  be  maintained  or  even 
increased.  In  the  myocarditis  of  old  age  the  exciting  cause  is,  as  a  rule, 
sclerosis  of  the  coronary  vessels.  Being  a  part  of  general  arterio-sclerosis, 
the  blood-pressure  is  high.  In  obese  individuals  with  fatty  overgrowth 
of  the  heart,  the  blood-pressure  is  usually  high. 

Percussion. — The  cardiac  outline  may  be  normal  or  but  slightly  in- 
creased in  the  transverse  diameter  but  if  dilatation  is  present,  cardiac 
dulness  will  be  increased  both  to  the  right,  to  the  left,  or  both. 

Auscultation. — The  heart  sounds  are  distant  and  feeble  and  at  times 
scarcely  audible.  The  first  sound  is  short  and  sharp  and  lacks  the  normal 
muscle  tone.  The  aortic  or  pulmonic  second  sound  may  be  accentuated. 
A  soft  blowing  systolic  murmur  is  often  present  at  the  apex  due  to  relative 
insufficiency  of  the  mitral  valve.  It  tends  to  disappear  with  rest  and 
appropriate  treatment.  On  the  other  hand,  it  is  often  possible  to  bring 
out  such  a  murmur  by  having  the  patient  ascend  a  flight  of  stairs  or  walk 
up  and  down  the  room  for  a  few  minutes.  A  murmur  developing  under 
these  circumstances  is  practically  always  an  evidence  of  muscular  insuf- 
ficiency. There  may  be  a  tricuspid  murmur  and  a  positive  venous  pulse 
due  to  relative  insufficiency  and,  in  not  a  few  cases,  there  is  a  systolic 


DISEASES    OF    THE    MYOCARDIUM  633 

murmur  at  the  aortic  area  due  to  sclerosis  or  dilatation  of  the  first  part  of 
the  aorta. 

Diagnosis. — Chronic  degeneration  of  the  myocardium  can,  in  some 
instances,  be  recognized  with  reasonable  certainty.  In  other  instances  its 
presence  is  a  matter  of  inference  as  unequivocal  evidence  cannot  be  ob- 
tained. Patients  in  whom  a  diagnosis  of  chronic  myocarditis  seems  to  be 
justified  are,  as  a  rule,  individuals  past  the  middle  period  of  life  who 
develop  symptoms  characteristic  of  cardiac  insufficiency.  On  examina- 
tion the  transverse  diameter  of  cardiac  dulness  is  increased,  the  first 
sound  is  feeble  and  valvular  in  character  and  associated  with  it  there  is 
often  a  soft,  blowing  systolic  murmur.  The  second  aortic  sound  may  be 
accentuated  and  ringing. 

The  type  of  case  which  too  commonly  escapes  recognition  is  that  in 
which  symptoms  are  absent  or  too  trivial  to  demand  attention.  This  is 
the  type  in  which  sudden  death  is  often  the  first  intimation  that  serious 
cardiac  disease  is  present.  Babcock  states  that  myocardial  damage  may 
be  strongby  suspected  in  individuals  of  or  beyond  middle  age  who  have 
dissipated,  overindulged  themselves  at  the  table,  or  lived  at  high  pressure. 
The}-  will  often  be  found  to  have  a  high  blood-pressure,  arteries  which  are 
visibly  and  palpably  thickened  and  albumen  and  casts  in  the  urine. 
Examination  of  the  heart  will  show  some  increase  in  dulness  to  the  left, 
an  intensely  accentuated  second  aortic  sound,  and  accentuation  of  and  a 
valvular  quality  of  the  first  sound  at  the  apex.  A  harsh  systolic  murmur 
at  the  aortic  area  is  a  frequent  finding  (see  p.  730). 

It  is  well  to  bear  in  mind  that  the  etiology  and  symptomatology  of 
chronic  degeneration  of  the  myocardium  and  the  blood-vessels  are  often 
essentially  the  same  and  that  the  presence  of  one  almost  invariably  im- 
plies the  other. 

ANEURISM  OF  THE  HEART 

Aneurism  of  the  heart  wall  may  occur  in  an  acute  and  a  chronic  form. 
The  acute  type  is  a  sequel  to  ulcerative  endocarditis  and  usually  termi- 
nates by  perforating  into  the  pericardial  sac.  It  is  of  pathological  in- 
terest only. 

Etiology. — The  condition  is  rare.  In  a  study  of  9940  autopsy  records 
at  the  Pennsylvania  and  Philadelphia  General  Hospitals,  Norris  found 
8  cases.  In  1908  M'Elroy1  found  there  had  been  recorded  in  medical 
literature  300  cases.  Cardiac  aneurism  is  practically  always  a  sequel  of 
chronic  fibroid  myocarditis. 

Morbid  Anatomy. — The  condition  is  usually  single  although  occasion- 
all}'  more  than  one  has  been  noted.  The  aneurism  is  nearly  always 
located  in  the  anterior  part  of  the  left  ventricle  near  the  apex  and  usually 
consists  of  a  globular  distention  in  this  region  (Fig.  370).  At  the  point 
of  bulging  the  heart  wall  is  greatly  thinned  and  fibrous  in  character. 
The  ventricle  elsewhere  is  usually  h}Tpertrophied.  The  endocardium 
lining  the  aneurism  is  often  thickened,  opaque  and  may  show  calcareous 
plaques.  The  aneurismal  sac  may  be  filled  with  a  thrombus.  If  the 
opening  into  the  ventricle  is  narrow  a  thrombus  usually  forms  and  this 
tends  to  relieve  the  strain  on  the  thin  and  weakened  wall.  In  the  ma- 
jority of  cases,  however,  the  strain  proves  too  great  and  rupture  takes 

1  Jour.  Am.  Med.  Assoc,  Aug.  1,  190S. 


634 


DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


place.     The  size  of  the  aneurism  varies  greatly;  it  may  be  the  size  of  a 
fist  or  even  larger. 

Symptoms  and  Signs. — There  are  no  symptoms  which  can  be  at- 
tributed to  this  lesion.  Inasmuch  as  it  is  one  of  the  phases  of  chronic 
fibrous  myocarditis  the  symptoms  presented  will  be  those  occurring  in  the 
latter  condition.  If  it  is  to  be  recognized  at  all  it  will  be  by  the  presence 
of  a  pulsatile  tumor  situated  at  a  point  beyond  the  limits  of  the  aorta. 


Fig.  370. — Aneurism  of  the  left  ventricle.  The  left  ventricular  wall,  which  is  elsewhere 
hypertrophied,  is  markedly  attenuated  on  its  left  side  at  and  above  the  apex.  In  this 
region  a  marked  bulging,  about  the  size  and  shape  of  a  large  duck  egg,  is  seen.  The  endo- 
cardium in  this  region  is  covered  with  calcareous  plaques.  The  aortic  and  mitral  valves 
show  moderate  sclerosis.      {Specimen  from  the  Philadelphia  Hospital.) 

At  first  sight  the  condition  with  which  a  pulsatile  tumor,  due  to  a 
cardiac  aneurism,  is  most  apt  to  be  confused  is  a  pulsating  empyema. 
The  absence  of  signs  pointing  to  fluid  in  the  pleural  sac  and  failure  to 
obtain  pus  with  an  exploring  needle  serves  to  rule  out  empyema. 
Owing  to  the  enlargement  of  the  heart  and  the  change  in  its  contour  a 


DISEASES    OF    THE    MYOCARDIUM 


635 


cardiac  aneurism  may  simulate  a  pericardial  effusion  and  aspiration  be 
performed. 

The  following  case  was  seen  at  the  Pennsylvania  Hospital  on  the  serv- 
ice of  Dr.  J.  Norman  Henry. 

The  patient,  a  colored  woman,  aged  forty-two  years,  was  admitted  to  the  hospital 
complaining  of  extreme  shortness  of  breath,  weakness,  cough  and  swelling  of  the  legs. 
Her  husband  and  several  brothers  and  sisters  had  died  of  tuberculosis.  For  the  past 
three  years  she  had  had  a  cough  and  expectoration  and  occasional  night  sweats.  She 
had  been  married  eight  years  but  had  had  no  children  or  miscarriages.  Her  present 
illness  began  suddenly  with  dyspnea,  palpitation  and  edema  of  the  legs,  a  month  prior 
to  her  admission  to  the  hospital.  Her  cough  had  become  worse  and  for  two  months 
she  had  been  hoarse. 


Fig.   371. — Aneurism  of  left  ventricle.     {Patient  of  Dr.  J.N.  Henry.) 

Physical  Examination. — On  inspection  there  was  seen  in  the  left  axillary  region, 
at  the  level  of  the  eighth  rib,  a  pulsating  tumor  which  was  definitely  expansile  (see  Fig. 
14).  The  heart  was  displaced  to  the  right.  No  murmurs  were  heard.  Over  the 
lower  half  of  the  left  chest  the  percussion  note  was  flat,  the  breath  sounds  were  barely 
audible  and  vocal  fremitus  was  diminished.  The  Wassermann  reaction  was  strongly 
positive.  Fluoroscopic  examination  showed  the  presence  of  fluid  in  the  left  chest 
and  distinct  pulsation.  The  heart  and  trachea  were  much  displaced  to  the  right. 
Later  a  slight  effusion  was  present  on  the  right  side  also.  The  left  side  was  tapped  and 
900  c.c.  of  serous  fluid  withdrawn. 

The  diagnosis  seemed  at  first  to  lie  between  a  pulsating  empyema  and  an  aneurism. 
The  former  was  ruled  out  after  the  paracentesis  as  the  pulsation  persisted.     A  diagno- 


636  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

sis  of  aneurism  of  the  thoracic  aorta  was  untenable  because  of  the  location  of  the  pul- 
sating tumor. 

The  patient  died  six  months  after  admission  as  the  result  of  a  cerebral  hemorrhage. 
The  heart  (Fig.  371)  showed  the  presence  of  a  large  aneurism  in  the  left  ventricle  just 
posterior  to  the  apex  of  the  heart.  The  wall  of  the  aneurism  was  composed  of  fibrous 
tissue. 

MYOCARDIAL  CHANGES  DUE  TO  SYPHILIS 

Until  comparatively  recently  the  only  lesion  of  the  heart  that  could 
unmistakably  be  attributed  to  syphilis  was  the  gumma,  although  it  has 
always  been  recognized  that  syphilitic  subjects  were  prone  to  suffer  from 
degenerative  changes  of  the  heart  muscle.  These  changes,,  however, 
were  looked  upon  as  part  of  a  general  or  coronary  arterio-sclerosis.  Since 
the  discovery  of  the  spirocheta  pallida,  histological  studies  have  demon- 
strated that  this  organism  shows  an  especial  predilection  for  the  aorta 
and  heart.  It  is  now  clearly  proved  that  the  root  of  the  aorta  is  especi- 
ally vulnerable  and  that  in  niam1-  instances  the  aortic  valves  are  also 
implicated.  Furthermore,  the  studies  of  Warthin1  and  others  have 
shown  that  the  heart  muscle  itself  may  be  invaded  by  the  spirochetal  and 
that  the  infection  may  occur  in  the  early  stages  of  syphilis.  In  41  cases 
of  syphilis  studied  by  Warthin,  active  sj-philitic  lesions  were  found  in 
the  heart  muscle  in  36.  Heretofore  it  has  been  taught  that  syphilitic 
changes  in  the  heart  occurred  only  as  late  manifestations  of  the  disease. 
Morbid  Anatomy. — There  seems  to  be  a  selective  tendency  on  the 
part  of  the  spirocheta?  to  attack  the  coronary  vessels.  In  a  series  of  50 
cases  studied  b}^  Brooks2  the  coronary  arteries  in  35  showed  a  relatively 
severer  degree  of  change  than  the  remainder  of  the  arterial  system.  The 
early  syphilitic  changes  in  the  heart  have  been  studied  by  Brooks,3 
Adler4  and  Warthin.5  The  change  occurs  early  in  the  course  of  the  in- 
fection and  involves  the  terminals  of  the  coronary  system.  The  first 
alteration  consists  of  an  infiltration  of  mononuclear  cells  in  the  muscle 
about  the  vessels  and  in  addition  there  are  numerous  spirocheta?.  This 
is  followed  by  cellular  fibrosis  and  finally  necrosis.  Brooks  urges  the 
importance  of  bearing  in  mind  the  character  of  the  lesion  and  the  fact 
that  it  may  manifest  itself  during  the  so-called  secondaiy  period.  Vigor- 
ously treated,  such  lesions  may  be  recovered  from  without  permanent 
damage  being  clone  to  the  heart.  Neglected,  there  may  eventually  result 
areas  of  fibrosis  or  the  formation  of  gummata-. 

.  The  late  cardiac  changes  due  to  syphilis  are  fairly  common.  In  an 
analysis  of  the  cardiac  lesions  found  in  50  consecutive  cases  of  syphilis 
Brooks  found  that  the  changes  in  the  heart  muscle  were  by  far  the  most 
common.  Fatty  degeneration  was  found  in  44;  fibroid  changes  occurred 
in  4  and  in  5  there  were  fibroid  changes  and  fatty  degeneration.  Gum- 
mata were  present  in  5  of  the  50  cases.  Mracek,6  among  60  cases,  found 
gummata  in  10.  In  common  with  degenerative  changes  due  to  other 
causes  sj^philitic  involvement  may  include  or  be  limited  to  the  specialized 
fibers,  known  as  the  auriculo-ventricular  bundle.     There  are  now  on 

1  Trans.  Assoc.  Am.  Phys.,  1914. 

2  International  Clinics,  Twenty-fifth  Series,  vol.  i,  1915. 

4  Trans.  Assoc.  Am.  Phys.,  1898. 

5  Ibid.,  1914. 

6  Arch.  f.  Dermatol,  und  Syph.,  1893,  xxv,  p.  279. 


DISEASES    OF   THE    MYOCARDIUM 


637 


record  a  number  of  cases  of  the  Adams-Stokes  syndrome  in  which  the 
bundle  of  His  was  the  site  of  a  gummatous  infiltration.  An  excellent 
example  of  this  is  shown  in  Fig.  372.  The  lesions  are  chiefly  encountered 
in  the  ventricles,  are  generally  multiple  and,  as  a  rule,  are  sharply  denned 
and  encapsulated  (see  Fig.  373).  Absorption  of  the  gumma  may  be 
followed  by  cardiac  fibrosis  or  aneurism. 

Symptoms. — The  symptoms  of  the  late  cardiac  manifestations  of 
syphilis  differ  in  no  particular  from  degenerative  changes  due  to  other 


Fig.  372. — The  nodular  gummatous  mass  obliterates  the  undefended  space  of  the  inter- 
ventricular septum,  and  entirely  fills  that  part  of  the  septum  through  which  the  auriculo- 
ventricular  bundle  runs.     {Specimen  from  the  Pennsylvania  Hospital.) 

causes.  It  is  not  generally  appreciated,  however,  that  the  heart  may  be 
affected  early  in  the  infection  and  that  at  this  time  the  evidences  of  severe 
cardiac  weakness  may  be  present.  Brooks  found  that  dyspnea  was  the 
most  common  symptom  in  the  early  cases.  Precordial  pain  and  tender- 
ness are  also  common  and  in  some  instances  anginal  attacks  are  frequent. 
Grassmann1  also  has  directed  attention  to  the  cardiac  symptoms  arising 

1  Munch,  med.  Woch.,  1897,  xliv;  Deut.  Arch.  f.  Klin.  Med.,  1900.  Ixix,  58.  264. 


638  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

in  early  syphilis.  He  found  that  dilatation  of  the  right  heart  was  com- 
mon and  that  a  functional  or  accidental  murmur  at  the  apex  was  present 
in  40  per  cent,  of  his  cases.  The  murmur  is  soft  and  blowing  in  character, 
becomes  more  evident  on  exercise  and  is  occasionally  transmitted  toward 
the  axilla.  In  addition,  alterations  in  the  cardiac  rhythm  are  almost  uni- 
versally present  in  the  form  of  arrhythmia,  bradycardia  or  tachycardia. 


Fig.  373. — Gumma  of  the  left  ventricle.      (Specimen  from  the  Pennsylvania  Hospital.) 

The  cardiac  involvement  may  be  severe  enough  to  cause  death  at  this 
time;  on  the  other  hand,  vigorous  antiluetic  treatment  usually  causes  a 
disappearance  of  the  symptoms. 

As  a  rule,  the  symptoms  of  the  late  cardiac  manifestations  of  syphilis 

differ  in  no  particular  from  degenerative  changes  due  to  other  causes. 

Sears1  believes  that  syphilis  should  be  suspected,  however,  in  apparently 

healthy  patients  who  as  the  result  of  overwork  or  some  sudden  exertion, 

1  Boston  Med.  &  Surg.  Jour.,  June  16,  1910. 


DISEASES    OF    THE    MYOCARDIUM  639 

suddenly  develop  urgent  cardiac  symptoms.  These  symptoms  may  con- 
sist of  tachycardia  accompanied  by  great  anxiety  and  mental  distress  or 
by  the  usual  signs  of  myocardial  insufficiency.  Severe  headache  and 
vomiting  may  be  early  symptoms.  A  striking  feature  of  these  cases  is 
their  failure  to  respond  to  the  ordinary  cardiac  tonics. 

Breitmann1  believes  that  many  supposedly  rheumatic  heart  affections 
are  in  reality  syphilitic  in  origin.  This  should  be  suggested  by  the  rapid 
onset  of  cardiac  symptoms,  with  or  without  fever,  in  the  midst  of  apparent 
health.  Death  may  occur  suddenly  or  the  cardiac  weakness  may  persist 
for  a  long  time  without  signs  of  valvular  mischief  and  without  being 
influenced  by  the  ordinary  heart  tonics. 

Diagnosis. — It  is  to  be  borne  in  mind  that  syphilis  may  attack  the 
heart  early  in  the  course  of  the  infection  and  for  this  reason  the  heart 
should  be  carefully  examined.  The  occurrence  of  cardiac  symptoms  or 
signs  at  this  time  demand  active  antiluetic  treatment.  The  recognition 
of  cardiac  syphilis  as  a  late  manifestation  is  dependent  on  establishing 
the  presence  of  an  acquired  or  congenital  infection.  In  some  instances 
it  is  frankly  acknowledged  that  such  an  infection  has  occurred;  in  others 
it  is  denied.  In  the  absence  of  syphilitic  stigmata  the  Wasserrnann  test 
is  our  main  reliance.  Syphilis  is  to  be  suspected  if  cardiac  symptoms 
suddenly  develop  in  young  or  middle-aged  individuals  who  have  been 
healthy  previously. 

1  Bed.  Klin.  Woch\,  September  25,  1912. 


CHAPTER  XXVII 
ENDOCARDITIS 

ACUTE  ENDOCARDITIS 

While  any  portion  of  the  endocardium  may  become  the  seat  of  inflam- 
matory changes  the  term  " endocarditis"  is  usually  understood  to  refer  to 
the  valves.  It  is  to  be  borne  in  mind,  however,  that  the  inflammatory' 
process  may  involve  the  mural  endocardium  independently  or  as  the  result 
of  extension  from  the  valves.  In  like  manner  an  acute  aortitis  may  arise 
as  the  result  of  a  concomitant  infection  of  the  semilunar  valves. 

Two  types  of  acute  endocarditis  are  commonly  considered,  namely, 
simple  and  malignant.  It  is  generally  recognized,  however,  that  the 
classification  is  an  arbitrary  one  and  that  no  sharp  dividing  line  can  be 
drawn.  Simple  acute  endocarditis  has  been,  and  is  still  sometimes  re- 
ferred to  as  benign.  The  designation  is  a  bad  one  and  should  not  be 
employed,  as  it  conveys  the  impression  that  a  large  group  of  cases  of  endo- 
carditis may  suffer  from  no  serious  after-effects.  It  cannot  be  too  strongly 
impressed  upon  the  mind  that  simple  endocarditis  is  always  fraught  with 
danger  and  that  more  people  ultimately  die  as  the  result  of  such  an 
occurrence  than  is  the  case  with  the  more  serious  malignant  or  infective 
type  of  the  disease.  Although  we  clearly  recognize  the  fact  that  the  dis- 
tinction between  the  simple  and  the  malignant  types  of  the  disease  is 
largely  one  of  severity,  there  are,  at  the  same  time,  certain  etiological 
and  clinical  differences  which  makes  a  separate  description  of  the  two 
processes  advisable. 

Acute  Simple  Endocarditis 

Etiology. — This  type  of  the  disease  occurs  more  often  in  childhood 
and  adolescence  than  in  any  other  period  of  life,  largely  because  of  the 
frequence'  of  attacks  of  acute  rheumatic  fever  in  early  life.  So  commonly 
does  acute  endocarditis  develop  as  the  result  of  rheumatic  fever  that  it 
is  sometimes  termed  rheumatic  endocarditis.  Prior  to  the  age  of  puberty, 
rheumatic  attacks  are  almost  constantly  associated  with  the  endocar- 
dial lesions.  The  following  table  compiled  by  Cowan1  indicates  the 
extraordinary  frequenc3r  with  which  the  two  conditions  co-exist: 

I    Cases  of  acute  rheumatism  Cases  of  endocarditis 

Gibson 325  161 

Macrae 300  105 

Church 889  494 


Moore.  . 
Latham . 


100  90 

136  74 

1750  933 


1  ''Diseases  of  the  Heart,"  1914. 
640 


ENDOCARDITIS  641 

These  figures,  which  show  that  53.3  per  cent,  of  the  cases  developed  an 
acute  endocarditis,  serve  to  emphasize  the  important  relationship  that 
acute  rheumatic  fever  bears  to  cardiac  disease.  As  a  rule,  the  endocarditis 
develops  during  the  first  attack  of  rheumatism  and  the  valvular  damage 
is  apt  to  be  increased  if  subsequent  attacks  occur.  The  endocarditis  may 
manifest  itself  as  early  as  the  second  day  of  the  rheumatic  attack  or  it 
may  be  delayed  until  the  inflammatory  symptoms  have  entirely  subsided. 
The  frequency  of  the  endocarditis  bears  no  relation  to  the  severity  of 
the  arthritis.  An  extremely  severe  attack  of  rheumatism  may  not  involve 
the  endocardium;  on  the  other  hand,  a  trifling  and  mild  attack  may  cause 
serious  endocardial  mischief. 

Closely  allied  to  the  rheumatic  type  of  endocarditis  is  that  which 
follows  attacks  of  tonsillitis.  The  importance  of  tonsillitis  as  a  cause  of 
endocarditis  is  now  fully  recognized.  Very  often  the  tonsillar  attacks 
are  very  mild  and  pass  for  nothing  more  than  a  slight  sore  throat.  It  is 
quite  possible  that  many  cases  of  endocarditis,  in  which  there  is  no  ap- 
parent etiological  factor,  have  had  their  origin  in  attacks  of  mild  and  un- 
recognized tonsillitis  or  acute  rheumatic  fever.  In  children  suffering  from  a 
chronic  valvular  lesion,  careful  questioning  will  sometimes  reveal  a  his- 
tory of  vague  and  fugitive  joint  pains  which  at  the  time  of  their  occur- 
rence caused  little  or  no  concern. 

Xext  to  rheumatic  fever  the  most  frequent  cause  of  endocarditis  is  cho- 
rea. "Valvular  lesions  are  extremely  common  in  choreic  patients,  and 
were  present  in  262  out  of  829  patients  who  were  examined  during  or 
after  illness"  (Cowan). 

Any  of  the  acute  infectious  diseases  may  give  rise  to  an  endocarditis, 
but  with  the  exception  of  croupous  pneumonia  such  an  occurrence  is  not 
common.  Not  infrequently  acute  endocarditis  is  noted  in  phthisis, 
cancer,  gout,  diabetes  and  Bright's  disease.  The  condition  is  practically 
always  a  secondary  one  and  even  in  those  instances  in  which  a  primary 
infecting  focus  cannot  be  discovered  it  is  now  held  that  this  undoubtedly 
is  present.  Recent  bacteriological  studies  indicate  that  in  the  majority  of 
cases  of  active  endocarditis  a  streptococcus  bacteremia  is  present. 

Morbid  Anatomy. — Except  when  the  endocarditis  arises  during  intra- 
uterine life  the  valves  of  the  left  heart  are  the  ones  which  are  almost  in- 
variably affected.  When  a  valvulitis  arises  as  the  result  of  some  infectious 
or  toxic  agent,  the  inflammatory  process  occurs  in  certain  definite  areas. 
The  mitral  leaflets  are  more  frequently  involved  than  the  aortic.  Sibson 
has  offered  the  explanation  that  the  increased  liability  of  the  mitral  valve 
is  due  to  the  fact  that  the  edges  of  the  leaflets  of  this  valve  are  closed  with 
much  greater  tension  than  is  the  case  with  the  aortic  valve.  The  mitral 
leaflets  are  subject  also  to  a  wider  range  of  play — wider  excursions,  there- 
fore, produce  more  wear  and  tear.  The  endocardial  changes  as  they 
occur  in  the  valves  take  place  on  the  auricular  surface  of  the  mitral  and 
the  ventricular  surface  of  the  aortic  due  to  the  fact  that  these  surfaces 
are  bathed  by  the  blood  stream.  The  lesions  are  located  just  behind 
the  free  edges  of  the  valves. 

The  first  evidence  of  the  inflammatory  change  is  a  slightly  swollen 
appearance  of  the  affected  area  and  a  faint  hyperemia  due  to  the  increased 
vascularity  of  the  part.  This  is  followed  by  a  shedding  of  the  endothelial 
and  subendothelial  cells,  which  gives  rise  to  a  grayish,  opaque  appearance. 
Over  the  site  of  these  degenerated  areas  fibrin  is  deposited  in  the  form  of 


642  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

small  bead-like  excrescences  or  granulations  (endocarditis  verrucosa). 
The  size  of  the  growths  vary  greatly;  they  may  become  sufficiently  large 
to -prevent  closure  of  the  valve  or  obstruct  the  blood  stream.  Tangled 
in  the  meshes  of  the  fibrinous  deposits  bacteria  are  found,  although  this 
is  more  commonly  the  case  in  the  malignant  than  the  simple  form  of  the 
disease.  In  the  majority  of  instances  of  simple  endocarditis  no  bacteria 
are  found;  this  is  especially  true  of  the  affection  as  encountered  in  the 
chronic  wasting  diseases. 

In  addition  to  the  involvement  of  the  valves  the  chordae  tendineae 
may  be  implicated  and  later  become  shortened  as  the  result  of  contracting 
scar  tissue. 

It .  is  now  recognized  that  an  acute  endocarditis  is  almost  always 
accompanied  by  myocardial  change.  The  myocardial  change  may  be 
general  or  it  may  be  limited  to,  or  most  marked  in,  the  muscle  tissue  at 
the  base  of  the  affected  valve.  The  myocardial  change  may  be  very 
mild  and  trivial  and  give  rise  to  no  evidence  of  its  existence.  On  the 
other  hand,  disturbances  of  rhythm  may  occur  as  the  result  of  implication 
of  Tawara's  node  or  the  bundle  of  His.  In  a  very  fair  proportion  of  cases 
of  acute  endocarditis  there  is  also  an  associated  pericarditis. 

Simple  acute  endocarditis  is  of  itself  not  serious.  The  acute  inflam- 
matory stage  is  rarely  intense  enough  to  destroy  tissue  and  emboli  rarely 
arise  from  the  vegetations.  Its  great  danger  lies  in  the  after-results. 
With  the  subsidence  of  the  acute  stage  granulation  tissue  is  formed  and 
this  organizes  into  scar  tissue.  With  the  retraction  of  the  scar  tissue  the 
edge  of  the  valve  may  be  curled  back  giving  rise  to  incompetency  or  the 
leaflets  may  become  ankylosed  producing  a  stenosis.  Another  very  serious 
danger  is  the  fact  that  these  fibrous  patches  on  the  valves  are  very  prone 
to  become  reinfected  with  either  the  simple  or  malignant  form  of  the 
disease.  Malignant  endocarditis  is  very  commonly  engrafted  on  an  old 
chronic  valvular  defect. 

Symptoms.— There  are  no  distinctive  symptoms  of  acute  simple  en- 
docarditis; indeed,  they  may  be  wanting  entirely.  In  a  very  large  pro- 
portion of  cases  the  cardiac  lesion  is  masked  by  the  primary  infection. 
Fever  is  probably  the  most  important  symptom  referable  to  the  endocar- 
ditis. It  is  not  always  easy,  however,  to  determine  its  significance  as 
fever  is  already  present  as  a  result  of  the  rheumatic  attack,  pneumonia  or 
other  acute  infection.  One  should  be  suspicious  of  endocardial  involve- 
ment if  the  temperature  changes  in  character  or  if,  after  a  period  of  nor- 
mal temperature,  fever  again  develops.  In  some  cases  there  may  be  a 
sense  of  precordial  oppression  or  actual  pain  and  in  others  there  may  be 
palpitation  of  the  heart. 

Physical  Signs. — I  have  already  alluded  to  the  great  frequency  with 
which  acute  endocarditis  is  associated  with  rheumatic  fever.  As  an 
etiological  factor  it  overshadows  all  others,  especially  in  young  children. 
It  is  essential  to  keep  this  in  mind  and  to  take  the  precaution  of  examining 
the  heart  daily  as  in  the  absence  of  symptoms  a  cardiac  lesion  may  very 
easily  escape  notice.  Owing  to  the  very  serious  after-effects  which  may 
arise,  even  from  a  trivial  lesion,  it  is  incumbent  upon  us  to  detect  the 
trouble  as  early  as  possible  so  as  to  prevent  any  undue  strain  being  put 
upon  the  heart  until  the  acute  stage  of  the  disease  has  passed. 

Inspection. — In  the  presence  of  acute  rheumatic  fever  inspection  of  the 
precordium  should  be  carefully  made  each  day  as  by  this  one  procedure 


ENDOCARDITIS  643 

most  valuable  information  may  be  obtained.  While  no  abnormality 
may  be  noted  throughout  the  course  of  the  disease  there  will  often  be  seen 
a  gradual  displacement  of  the  apex  beat  beyond  the  nipple  line;  or  the 
cardiac  impulse  may  be  forcible;  or  instead  of  a  forcible  heaving  impulse 
it  may  be  diffuse  and  wavy  in  character. 

Palpation. — This  will  confirm  the  character  of  the  impulse  noted  on 
inspection.  In  addition,  the  shock  of  both  the  first  and  second  sounds 
may  be  felt. 

The  character  of  the  pulse  should  be  carefully  noted  as,  in  not  a  few 
cases,  it  furnishes  the  only  clue  pointing  to  a  cardiac  lesion.  The  pulse 
may  be  unduly  accelerated  in  proportion  to  the  degree  of  fever  or  it  may 
remain  high  after  the  primary  infection  has  subsided.  Go  wan  has 
pointed  out  that  the  administration  of  the  salicylates  will  often  slow  the 
pulse  rate  and  that  after  these  drugs  are  discontinued  the  pulse  rate  will 
increase  in  frequency  if  an  endocarditis  is  present.  In  some  cases  the 
pulse  is  unduly  slow.  Irregularity  of  the  pulse  is  also  of  great  importance. 
The  irregularity  may  be  due  to  a  temporary  heart  block,  to  extrasystoles 
or  auricular  fibrillation. 

Percussion. — The  information  obtained  by  percussion  of  the  precor- 
dium,  in  cases  of  acute  endocarditis,  is  not  great.  There  may  be  some 
increase  in  the  area  of  cardiac  dulness  upward  and  to  the  left  and  occa- 
sionally to  the  right. 

Auscultation. — The  most  constant  sign  and,  at  the  same  time,  the 
most  reliable  evidence  of  acute  endocarditis  is  a  systolic  murmur  at  the 
apex.  The  greater  frequency  of  apical  as  compared  to  aortic  murmurs  is 
due  to  the  fact  that  in  the  great  majority  of  cases  of  simple  endocarditis 
the  rheumatic  infection  affects  by  preference  the  mitral  valve.  The  mur- 
mur may  occur  within  a  few  days  of  the  onset  of  the  rheumatic  attack  or 
it  may  not  be  heard  until  convalescence  is  established.  Then  again,  it 
may  be  heard  first  some  weeks  or  months  after  complete  recovery.  In 
other  instances  a  murmur  may  be  heard  during  the  height  of  the  febrile 
attack,  then  disappear,  and  again  recur  as  the  result  of  a  chronic  endo- 
carditis. In  such  cases  it  is  possible-that  the  vegetations  interfere  with 
proper  closure  of  the  valve  and  as  these  are  absorbed  the  murmur  dis- 
appears, or,  what  is  more  probable,  the  murmur  is  caused  by  the  associ- 
ated myocarditis.  The  recurrence  of  a  permanent  murmur  is  caused  b}^ 
contraction  of  the  scar  tissue  which  distorts  the  leaflets  or  causes  their 
adherence,  with  the  result  that  a  leakage  or  obstruction  is  caused. 

The  time  of  the  murmur  in  acute  endocarditis  is  always  systolic;  it  is 
only  when  a  chronic  endocarditis  is  established  that  a  murmur  indicative 
of  obstruction  is  heard.  While  the  first  indication  of  trouble  may  be  a 
soft  blowing  murmur  it  will  be  noted,  if  the  heart  is  examined  from  day  to 
day,  that  the  initial  change  is  usually  a  blurring  of  the  first  sound;  later 
the  first  sound  becomes  roughened  in  character  or  sharply  accentuated 
and  finally  a  murmur  is  heard.  Associated  with  the  murmur  is  an  accen- 
tuation of  the  pulmonic  second  sound.  If  the  murmur  is  truly  organic,  it 
will  be  heard  best  at  the  apex  and  is  transmitted  towards  the  left  axilla. 
In  determining  whether  the  murmur  is  organic  or  functional  in  character 
it  must  be  borne  in  mind  that  in  acute  rheumatic  fever  a  marked  secondary 
anemia  is  sometimes  rapidly  established  and  this  may  cause  a  functional 
systolic  murmur  at  the  apex  or  base  of  the  heart.  Very  often  it  is  not 
possible  at  once  to  decide  the  question  and  it  is  onty  later  when  other 


644  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

signs  appear  that  one  can  be  certain  that  the  murmur  is  organic  in  nature. 
While  an  organic  murmur  may  vary  in  intensity  from  day  to  day,  one  of 
its  characteristic  features  is  to  gradually  become  more  and  more  evident. 

In  the  presence  of  fever  it  is  not  uncommon  to  hear  a  systolic  murmur 
at  the  pulmonic  area  which  is  without  significance.  Finally  there  may  be 
a  cardio-respiratory  murmur  (see  p.  247). 

Less  commonly  the  changes  described  above  are  heard  over  the  aortic 
area  or  both  valves  may  be  involved  simultaneously.  In  some  instances 
there  may  be  a  pericardial  friction  rub. 

MALIGNANT    ENDOCARDITIS 

(Septic,  Infective,  Ulcerative  or  Pernicious  Endocarditis) 

Etiology. — This  form  of  the  disease  rarely  develops  in  the  course  of 
acute  rheumatic  fever  or  chorea.  In  the  great  majority  of  instances  it 
arises  as  the  result  of  a  septic  wound,  puerperal  sepsis,  erysipelas,  a  gonor- 
rheal infection  or  some  inflammatory  disease  of  the  lungs,  notably  pneu- 
monia. Some  one  of  the  various  tjTpes  of  the  streptococcus  is  by  far  the 
commonest  organism  recovered  from  the  lesions.  Among  the  rarer  bac- 
teria may  be  mentioned  the  bacillus  of  diphtheria  and  influenza,  the 
meningococcus  and  staphylococcus. 

Malignant  endocarditis  is  rare  in  young  children;  the  great  majority 
of  cases  occur  in  young  adults  or  those  in  middle  life.  This  is  probably 
accounted  for  by  the  fact  that  the  septic  form  of  the  disease  very  fre- 
quently occurs  in  valves  previously  damaged  bj-  an  attack  of  acute 
rheumatic  fever. 

Morbid  Anatomy, — The  initial  changes  in  the  infective  type  of  endo- 
carditis may  present  the  same  appearance  as  is  seen  in  the  simple  form  of 
the  disease.  Usually,  however,  the  lesions  become  more  marked;  the 
excrescences  are  much  larger  and  in  extreme  cases  may  be  the  size  of  a 
cherry  (vegetative  endocarditis)  (see  Figs.  374  and  375).  The  largest 
vegetations  are  apt  to  occur  when  the  infecting  organism  is  either  the 
pneumococcus  or  the  gonococcus.  If  the  vegetations  are  broken  off,  an 
ulcerated  surface  is  left  which  may  perforate  the  valve  or  produce  a 
valvular  aneurism. 

In  another  type  of  the  disease,  known  as  endocarditis  ulcerosa,  the 
first  stage  shows  a  small,  somewhat  opaque,  yellow  patch,  with  a  slightly 
uneven  surface.  In  parts  of  such  patches  there  may  be  a  loss  of  substance. 
Over  these  ulcers  there  ma}^  be  deposited  reddish-gray  thrombotic  masses, 
which,  when  removed,  will  show  the  underlying  tissue  to  be  swollen, 
ulcerated  and  yellowish  in  color  (Adami  and  Nicholls). 

In  some  instances  the  infection  may  spread  to  the  wall  of  the  heart 
where  similar  changes  occur  in  the  mural  endocardium  (see  Fig.  376). 

Cultures  taken  from  the  ulcers  or  vegetations  will  show  large  numbers 
of  microorganisms  which  are  often  extremely  virulent.  A  histological 
examination  of  the  affected  area  will  also  show  countless  bacteria. 

According  to  Horder1  a  culture  of  a  pathogenic  organism  can  be  ob- 
tained in  90  per*  cent,  of  cases  of  infective  endocarditis.  In  addition  in 
a  very  high  percentage  of  cases,  the  infecting  organism  can  be  obtained 
from  the  circulating  blood.  In  by  far  the  largest  proportion  of  cases  the 
cause  of  the  trouble  is  a  streptococcus. 

1  Quarterly  Jour.  Med.,  vol.  ii,  p.  289. 


ENDOCARDITIS 


645 


The  frequency  with  which  the  different  valves  are  affected  is  as  fol- 
lows: the  mitral,  aortic,  mitral  and  aortic  together,  the  tricuspid  and  the 
pulmonary.  Involvement  of  the  mural  endocardium  is  also  frequently 
noted. 


FlG.  374. — Acute  infective  mitral  and  mural  endocarditis.  The  mitral  valve  is  covered 
with  Large  vegetations.  ■  Several  of  the  chorda:  tendineie  have  been  destroyed  by  ulcera- 
tion, only  short  unattached  stumps  remaining.  Vegetations  are  also  seen  on  the  mural 
endocardium.     {Specimen  from  the  Pennsylvania  Hospital.) 


One  of  the  niosl  striking  features  of  malignant  endocarditis  is  the 
occurrence  of  an  embolism.  This  is  not  surprising  when  we  recall  the 
soft,  friable  nature  of  the  valvular  vegetations.  As  the  lesion  progresses 
and  necrosis  sets  in  small  pieces  are  whipped  off  by  the  blood  current 
and  carried  to  some  distant  point .  The  viscera  most  commonly  involved 
are  the  spleen,  kidneys  and  brain,  but  no  portion  of  the  body  is  exempt. 


646  DISEASES    OF   THE    PERICARDIUM,    HEART,    AND    AORTA 

Occasionally  mycotic  aneurisms  involving  the  larger  vessels  have  their 
origin  in  this  way.     If  the  valves  in  the  right  heart  are  involved  there 


Fig.  375. — Acute  infective  endocarditis.  Showing  extensive  ulceration  of  the  aortic 
valves.  About  the  center  of  the  aortic  orifice  a  match-stick  projecting  from  a  thrombotic 
mass  indicates  the  course  of  the  perforation  in  the  aortic  leaflet.  {Specimen  from  the  Phila- 
delphia Hospital.) 

may  be  infarcts  in  the  lungs.     Owing  to  the  infective  nature  of  the  emboli 
the  resulting  infarcts  commonly  terminate  in  abscess  formation. 
In  some  instances  the  embolic  phenomena  are  absent. 


ENDOCARDITIS 


647 


Symptoms. — The  clinical  features  of  septic  endocarditis  do  not  lend 
themselves  readily  to  description.  In  some  instances  the  true  nature  of 
the  trouble  can  be  surmised  without  much  difficulty,  but  in  a  very  con- 
siderable proportion  of  cases  the  endocardial  lesion  is  masked  by  the 
primary  disease,  such  as  puerperal  sepsis,  pneumonia,  etc. 

"It  may  be  questioned  whether  it  is  worth  while  to  consider  the  pro- 
tean aspects  of  this  infection  under  diseases  of  the  heart,  since  the  mani- 


Fig.  376. — Acute  mural  endocarditis: 


festations  are  those  of  septicopyemia;  and  in  a  great  majority  of  all  cases 
the  features  of  the  general  infection  dominate  the  picture"  (Osier). 

Although  the  onset  is  varied  and  often  ill-defined,  the  process  when 
once  established  presents,  in  the  majority  of  cases,  certain  general  features. 
These  are,  an  irregular  type  of  fever,  sweating,  delirium,  progressive 
anemia,  loss  of  weight,  a  change  in  the  character  of  the  cardiac  murmurs 
and  the  occurrence  of  emboli. 


648 


DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


The  character  of  the  fever  is  variable.  It  may  be  remittent,  inter- 
mittent or  continued  in  type  (Fig.  377).  In  some  cases  it  is  paroxysmal, 
recurring  every  two  or  three  days  with  chills  and  drenching  sweats  thus 
resembling  malarial  fever.  The  fever  may  be  moderate  or  very  high 
but  no  matter  what  type  it  assumes  is  apt  to  be  irregular.  A  moderate 
amount  of  fever  of  the  continued  type  is  commonly  associated  with  endo- 
carditis superimposed  on  a  chronic  valvular  lesion.  Rarely  a  case  of 
septic  endocarditis  is  encountered  which  is  afebrile. 

The  embolic  phenomena,  although  sometimes  absent,  are  the  most 
certain  indication  of  septic  endocarditis.  The  spleen  is  the  organ  most 
frequently  involved  and  the  emboli  may  be  confined  to  this  viscus  alone. 


Temp. 
109 

108 

107 

106 

103 

H>  + 
103 
102 
101 
1O0 
99 
98 
9T 
96 


1    s 


tm 


Fig.  377. — Malignant  endocarditis. 


An  embolus  in  the  spleen  manifests  itself  by  sudden  pain  in  the  left  side, 
tenderness  on  pressure  and  enlargement  of  the  organ.  When  the  kidneys 
are  affected  there  are  renal  pain  and  bloody  urine.  Convulsions,  hemi- 
plegia, or  aphasia  may  follow  an  embolus  in  the  brain  and  visual  defects 
may  occur  if  one  of  the  retinal  vessels  is  involved.  Small  petechial  spots 
may  appear  in  the  skin  as  the  result  of  minute  emboli.  Occasionally  the 
embolus  blocks  one  of  the  larger  vessels  in  an  extremity  and  gangrene 
ensues.     If  the  lesion  is  right-sided,  emboli  may  be  carried  to  the  lungs. 

In  all  cases  of  suspected  septic  endocarditis,  providing  the  facilities 
are  available,  a  blood  culture  should  be  obtained.     A  lumbar  puncture 
should  also  be  made.     A  leukocytosis  is  usually  present- 
Generally  speaking,  septic  endocarditis  presents  itself  in  one  of  three 
ways:  (1)  The  phenomena  may  be  almost  entirely  cardiac  in  character; 


ENDOCARDITIS  649 

(2)  a  pyemic  form  in  which  there  isa  demonstrable  focus  of  infection;  and 

(3)  a  typhoid  form  in  which  the  infecting  focus  is  not  apparent. 

1.  The  cardiac  form  is  the  one  which  is  most  easily  recognized.  In 
this  type  of  the  affection,  the  patient,  already  suffering  from  a  chronic 
valvulitis,  develops  fever  of  a  continued  or  slightly  irregular  type,  an 
increase  in  the  cardiac  symptoms,  and  in  addition  there  may  be  an  em- 
bolism. The  attack  may  be  very  acute  or  may  be  relatively  mild  and 
persist  for  many  weeks.  Recurrences  are  common  and  recovery  often 
occurs. 

2.  In  the  pyemic  form  the  endocarditis  is  but  an  incident  in  the  general 
infection.  Its  recognition  is  always  attended  with  considerable  difficulty 
and  it  often  escapes  notice  entirely  owing  to  the  absence  of  a  murmur  or 
other  cardiac  signs.  Chills,  sweating,  irregular  fever,  anemia  and  wasting 
are  characteristic  of  a  general  sepsis  and  while  involvement  of  the  endo- 
cardium may  aggravate  these  symptoms,  one  cannot  make  a  diagnosis  of 
endocarditis  in  the  absence  of  a  murmur,  cardiac  dilatation  or  embolic 
phenomena.  If,  in  the  course  of  general  sepsis  following  an  external 
wound  or  the  puerperium,  there  develops  a  loud  murmur  or  a  murmur 
previously  present  increases  in  intensity  or  changes  in  quality,  the  assump- 
tion that  the  heart  valves  have  been  included  in  the  infection  is  nearly 
always  warranted.  Dilatation  of  the  heart  in  the  course  of  septicemia 
also  points  to  cardiac  involvement.  In  the  absence  of  cardiac  signs  the 
occurrence  of  an  embolism  furnishes  ample  evidence  as  to  the  existence 
of  an  endocarditis. 

3.  The  typhoid  form  is  by  far  the  most  common  type  of  malignant  en- 
docarditis and  the  one  attended  with  the  greatest  difficulty  in  its  recogni- 
tion. In  this  form  we  lack,  as  a  rule,  the  presence  of  an  old  valvulitis 
or  a  demonstrable  focus  of  infection  to  arouse  our  suspicions.  The 
following  symptoms  are  common  to  both  typhoid  fever  and  septic  endo- 
carditis: a  continuous  type  of  fever,  progressive  exhaustion,  anemia,  a  low 
muttering  type  of  delirium,  enlargement  of  the  spleen,  diarrhea,  a  dry 
tongue  and  sordes.  In  addition,  petechial  and  other  skin  rashes  are  not 
infrequent.  While  a  patient  with  septic  endocarditis  may  not  have  all 
these  symptoms,  the  occurrence  of  several  of  them  may  point  so  strongly 
to  typhoid  fever  that  the  true  nature  of  the  trouble  is  not  thought  of.  In 
other  cases  cerebral  symptoms  may  predominate  and  lead  to  a  diagnosis 
of  cerebro-spinal  or  basilar  meningitis.  Cardiac  signs  and  symptoms  may 
be  wanting  entirely  or  they  may  be  very  indefinite  in  character.  Embolic 
phenomena  are  less  common  in  this  type  than  in  the  others;  their  occur- 
rence often  clears  up  an  obscure  case  at  once.  The  disease  lasts  for  from 
two  or  three  weeks  to  three  months. 

This  type  of  endocarditis  is  very  frequently  due  to  a  pneumococcus,  or 
gonococcus  infection. 

Physical  Signs. — Plwsical  signs  referable  to  the  heart  may  be  absent 
or  very  indefinite.  The  patient  is  lethargic,  the  face  is  pale  and  sunken 
and  the  general  appearance  is  indicative  of  some  severe  infection.  Unless 
there  has  been  present  a  chronic  valvulitis  the  physical  signs  are  almost 
entirely  auscultatory  although  in  the  terminal  stages  evidences  of  cardiac 
dilatation  may  be  made  out.  Mackenzie  lays  great  emphasis  on  the  pulse 
in  doubtful  cases  associated  with  pyemia  and  puerperal  septicemia.  In 
these  cases  the  heart  may  show  but  little  change  except  that  the  heart 
sounds  are  feeble.     The  pulse  is  small,  soft,  easily  compressed  and  not 


650  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

necessarily  rapid,  although  the  rate  is  apt  to  be  higher  than  the  degree  of 
fever  warrants. 

The  presence  of  a  murmur  is  the  determining  factor  in  most  cases. 
The  murmur  may  be  very  faint  and  repeated  examinations  may  be  nec- 
essary to  determine  its  presence.  One  of  the  characteristics  of  a  murmur 
occurring  in  malignant  endocarditis  is  its  variable  character.  It  is  apt  to 
change  both  in  quality  and  intensity  from  day  to  day.  The  sudden 
appearance  of  a  musical  murmur  is  strongly  indicative  of  septic  endocardi- 
tis. A  murmur  of  this  character  is  caused  by  a  large  and  projecting  vege- 
tation. If  in  the  course  of  an  obscure  infection  a  murmur  due  to  chronic 
valvulitis  undergoes  changes  or,  in  addition  to  the  mitral  murmur,  a 
diastolic  murmur  at  the  aortic  area  develops  during  the  course  of  the 
disease,  one  should  be  alert  as  to  the  possibility  of  an  infectious  endocar- 
ditis. 

Diagnosis. — In  that  group  in  which  the  symptoms  are  largely  cardiac 
in  character  the  diagnosis  is  fairly  easy,  especially  if  there  is  known  to  be  a 
chronic  valvulitis  already  present.  In  such  cases  the  occurrence  of  fever, 
the  presence  of  a  murmur  which  is  subject  to  changes  from  day  to  day  and 
the  appearance  of  embolic  phenomena  point  unmistakably  to  septic  en- 
docarditis. 

In  the  pyemic  form  of  endocarditis  the  diagnosis  will  depend  largely  on 
the  detection  of  valvular  mischief.  The  endocarditis  is  simply  an  in^ 
cident  in  the  general  septic  process  and  unless  a  murmur  develops  or 
embolic  phenomena  occur  the  cardiac  element  will  pass  unnoticed.  As 
previously  stated  a  small,  soft  and  easily  compressed  pulse  is  significant 
in  these  cases  of  general  sepsis. 

When  the  septicemia  is  characterized  by  paroxysmal  attacks  of  chills, 
sweating  and  fever  the  condition  may  be  mistaken  for  malaria.  An 
examination  of  the  blood  and  the  presence  or  absence  of  the  malaria 
Plasmodium  or  a  leukocytosis  would  readily  decide  the  question.  The 
presence  of  a  positive  blood  culture  is  of  no  value  in  determining  the 
presence  of  endocardial  involvement,  although  such  a  finding  demands 
that  the  heart  be  carefully  examined. 

The  typhoid  form  gives  rise  to  the  greatest  confusion  and  in  any  given 
case  it  is  often  most  difficult  to  distinguish  between  malignant  endocardi- 
tis, typhoid  fever  and  acute  miliary  tuberculosis.  Marked  prostration, 
anemia,  wasting  and  the  so-called  typhoid  state  may  occur  in  all  three. 
The  temperature  seen  in  true  typhoid  may  be  atypical;  on  the  other 
hand,  that  in  endocarditis  and  miliary  tuberculosis,  while  subject  to  many 
variations,  may  closely  resemble  that  seen  in  typhoid.  Even  with  the 
presence  of  a  mitral  murmur  one  cannot  be  certain  that  it  is  not  functional 
in  character,  owing  to  the  exhaustion  and  anemia  common  to  all  these 
conditions.  In  the  absence  of  definite  cardiac  signs  the  diagnosis  may  be 
cleared  up  by  a  blood  culture  or  lumbar  puncture.  If  malignant  endo- 
carditis is  present,  a  blood  culture  will  show,  in  a  fairly  large  percentage  of 
cases,  the  infecting  organism,  usually  a  streptococcus,  pneumococcus  or 
gonococcus.  In  typhoid  fever,  blood  cultures  if  taken  early  in  the  disease 
will  frequently  show  Eberth's  bacillus.  A  positive  Widal  reaction  speaks 
for  typhoid  but  not  infrequently  it  also  occurs  in  miliary  tuberculosis. 
The  latter  condition  is  notoriously  difficult  to  recognize  in  adults  although 
relatively  easy  in  children.  The  lungs  may  be  studded  with  minute 
tubercles  and  yet  produce  no  physical  signs  until  the  terminal  stages. 


ENDOCARDITIS  651 

Choroidal  tubercles  are  frequently  cited  as  an  aid  in  the  diagnosis  but  I 
have  never  seen  a  case  in  which  they  were  recognized.  In  malignant 
endocarditis  there  is  usually  a  leukocytosis,  while  in  typhoid  fever  and 
miliary  tuberculosis  there  is  a  leukopenia  or  a  normal  white  count. 
Although  an  attack  of  the  typhoid  form  of  endocarditis  is  often  prolonged 
for  several  months  the  diagnosis,  in  many  cases,  may  never  be  cleared  up 
satisfactorily;  in  others,  the  appearance  of  embolic  phenomena  renders  the 
nature  of  an  obscure  infection  clear  (see  also  p.  375). 

Chronic  Infectious  Endocarditis 

This  condition,  first  described  by  Osier,  is  also  known  as  subacute 
bacterial  endocarditis,  chronic  malignant  endocarditis,  chronic  ulcerative 
endocarditis  and  endocarditis  lenta.  In  this  form  of  the  disease  the 
patients  are  the  subjects  of  a  chronic  valvulitis  which  is  often  well  com- 
pensated and  causes  little  or  no  trouble.  A  fresh  infection  is  superim- 
posed on  this  old  lesion,  thus  forming  the  focus  of  a  chronic  septicemia. 

With  a  few  exceptions  the  infecting  organism  is  an  atypical  coccus 
which  has  been  termed  the  endocarditis  coccus.  It  is  thought  that  this 
organism  is  derived  from  the  pneumococcus  (Rosenow,  Libman).  In  a 
few  instances  streptococci,  staphylococci  and  influenza  bacilli  have  been 
obtained  in  the  blood  cultures.  Libman1  has  reported  89  cases.  Blood 
cultures  were  studied  in  75  and  of  this  number  the  endocarditis  coccus  was 
obtained  in  71  and  the  influenza  bacillus  in  four. 

The  duration  of  the  disease  is  from  a  few  months  to  a  year  and  a  half. 
Occasionally  recovery  takes  place,  but  in  the  great  majority  of  cases  a 
fatal  issue  ensues. 

Morbid  Anatomy. — Libman,  who  has  had  a  large  experience,  describes 
the  pathological  changes  as  follows :  The  mitral  valve  is  the  seat  of  the 
lesion  in  about  two-thirds  of  the  cases  and  the  aortic  in  one-third.  A 
striking  feature  is  the  involvement  of  the  wall  of  the  auricle  and  the 
chordae  tendinae.  The  vegetations  are  yellowish,  greenish,  pinkish  or 
reddish  in  color  and  vary  greatly  in  .size.  When  the  aortic  valve  is 
involved,  the  vegetations  are  usually  few  and  of  small  size,  although 
occasionally  there  may  be  an  enormous  green  mass  which  almost  blocks 
the  orifice  (see  Fig.  378).  As  they  grow  older  the  vegetations  become 
firmer  and  grayish  in  color. 

When  the  mitral  valve  is  involved,  the  vegetations  spread  up  on  left 
posterior  wall  of  the  auricle  (see  Fig.  378).  The  chordae  tendinese  also 
may  be  covered  with  vegetations  and  may  become  torn  so  that  the  ends 
may  lie  loose  near  the  papillary  muscles.  When  the  aortic  valve  is  the 
seat  of  the  disease  the  vegetations  have  a  tendency  to  extend  down  over 
the  endocardium  and  over  the  ventricular  aspect  of  the  aortic  flap  of  the 
mil  ral  valve.     Occasionally  an  aneurism  of  the  valve  leaflets  may  develop. 

(  Vrebral  embolism,  uremia,  pneumonia  and  progressive  anemia  are 
the  common  terminations. 

Symptoms. — The  onset  is  often  insidious  and  without  definite  symp- 
toms. Very  often,  however,  the  initial  symptoms  are  definitely  referred 
to  the  heart,  as  for  instance,  shortness  of  breath  on  exertion,  palpitation, 
and  cough  which  is  sometimes  attended  with  blood-streaked  sputum. 

1  Trans.  Assoc  Am.  Pln/s.,  1012;  sec  also  ibid.,  1913.  Libman  and  Celler: 
Am.  Jour.  Med.  Sc,  October,  1910. 


652 


DISEASES  OF  THE  PERICARDIUM,  HEART,  AND  AORTA 


Fever  is  present  in  all  cases  (Fig.  379).  It  is  often  slight  but  in  the 
majority  of  cases  is  high  and  intermittent  in  the  late  stages  of  the  disease. 
If  splenic  infarcts  occur,  the  fever  is  apt  to  be  high  and  intermittent. 


Fig  378. — Subacute  infective  endocarditis.  Showing  large  thrombotic  masses  almost 
completely  occluding  the  aortic  orifice.  There  is  marked  left  ventricular  hypertrophy, 
and  sclerotic  patches  are  seen  on  the  aorta  above  the  sinus  of  Valsalva. 

Chills  and  sweating  may  occur  in  association  with  the  fever.     Loss  of 
weight  and  extreme  weakness  take  place  in  most  cases. 

Precordial  pain  or  a  sense  of  oppression  in  the  chest  is  often  noted. 
Pain  in  the  joints  is  not  uncommon  and  may  be  associated  with  slight 


ENDOCARDITIS 


653 


transitory  swellings.  A  purpuric  eruption  may  be  present  also.  Libman 
has  called  attention  to  an  important  diagnostic  sign,  namely,  tenderness 
over  the  lower  part  of  the  sternum.  The  lightest  tap  with  the  percussing 
finger  may  cause  marked  pain. 

An  important  diagnostic  feature  is  the  presence  of  small,  painful 
erythematous  nodules  in  the  skin  of  the  hands  and  feet.  These  cutaneous 
nodes  rarely  occur  except  in  this  form  of  endocarditis  and  are  considered 
by  Osier  as  being  pathognomonic.  Petechias  in  the  skin  and  conjunc- 
tival mucous  membrane  are  frequently  noted. 

Hematuria  occurs  in  a  few  cases  and  albumen  and  casts  are  found 
from  time  to  time.  The  leukocytes  are  not  often  increased  in  number. 
A  characteristic  feature  is  the  presence  of  a  more  or  less  marked  anemia 


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Fig.   379. — Temperature  chart  from  a  case  of  subacute  infectious  endocarditis. 

which,  in  many  cases,  is  progressive.  Libman  has  emphasized  the  peculiar 
sallow  or  waxy  color  of  the  face  in  these  cases.  Later  the  face  may  assume 
a  coffee-colored  tint.  In  cases  which  become  bacteria-free,  the  face  and 
other  portions  of  the  body  often  assume  a  diffuse  brown  color.  The 
spleen  is  enlarged  in  nearly  all  cases  and  is  easily  felt  on  palpation.  In 
some  instances  the  organ  is  enormously  enlarged. 

Physical  Signs. — Examination  of  the  heart  shows  in  every  instance 
the  presence  of  an  organic  murmur  either  at  the  aortic  or  mitral  orifice, 
usually  the  latter.  Aside  from  the  murmur  the  heart  may  show  no  change 
throughout  the  course  of  the  disease.  This  is  especially  true  when  the 
mitral  valve  is  involved.  If  the  aortic  valve  is  primarily  implicated,  the 
cardiac  changes  are  apt  to  be  more  noticeable.  In  some  cases  there  are 
progressive  cardiac  changes,  the  heart  gradually  dilates,  the  character  of 
the  mitral  murmur  changes  or  there  develops  under  observation  a  diastolic 
aortic  murmur. 

In  addition  to  the  bacterial  stage  Libman  describes  a  bacteria-free 
healing  and  a  bacteria-free  healed  stage.     The  latter  is  often  character- 


654  DISEASES    OF   THE    PERICARDIUM,    HEART,    AND    AORTA 

ized  by  tenderness  over  the  sternum  and  a  brownish  discoloration  of  the 
face  and  other  portions  of  the  body.  In  some,  slight  symptoms  occur 
intermittently;  in  others,  nephritis  develops  and  the  patient  dies  of 
uremia;  while  in  still  others,  the  anemia  persists  and  signs  of  failing  com- 
pensation develop. 

Diagnosis. — Chronic  infectious  endocarditis  is  to  be  thought  of  if  a 
patient,  the  subject  of  chronic  valvulitis,  develops  a  prolonged  fever, 
becomes  anemic,  gradually  fails  in  strength  and  if  during  the  course  of 
the  disease,  develops  small,  painful  erythematous  nodules  in  the  skin  of 
the  hands  or  feet.  Osier  emphasizes  the  fact  that  these  changes  may 
occur  without  any  additional  alteration  in  the  heart.  Individuals  suffer- 
ing from  vague  symptoms  of  the  neurasthenic  type  are  not  infrequently 
the  victims  of  a  subacute  bacterial  endocarditis.  Blood  cultures  should 
be  made  in  all  suspected  cases. 

In  the  bacteria-free  cases  the  marked  tenderness  over  the  lower  por- 
tion of  the  sternum  and  the  diffuse  brownish  discoloration  of  the  face 
and  other  portions  of  the  body  are  important  diagnostic  points. 

Chronic  Valvular  Disease  of  the  Heart 

Etiology. — Of  the  various  manifestations  of  cardiac  disease  chronic 
valvulitis  comprises,  by  far,  the  largest  group.  Statistical  studies  indi- 
cate that  valvular  disease  represents  about  80  per  cent,  of  the  lesions 
which  may  involve  the  heart. 

Chronic  valvulitis,  or,  as  it  is  more  commonly  termed,  chronic  heart 
disease,  is  slightly  more  frequent  among  females  than  males.  This  is  to 
be  ascribed  to  the  greater  frequency  of  acute  rheumatic  fever  and  chorea 
among  females.  Oille,  Graham  and  Detweiler1  emphasize  the  impor- 
tance of  tonsillitis  as  an  etiological  factor,  especially  in  children  and  young- 
adult  females.  Prior  to  the  fifth  year  chronic  endocarditis  is  uncommon 
but  beyond  this  age  period  the  incidence  gradually  increases.  The  major- 
ity of  instances  of  cardiac  failure  resulting  from  a  chronic  endocarditis 
are  encountered  between  the  eighteenth  and  fortieth  years.  After  middle 
life  the  incidence  of  cardiac  failure  due  to  valvular  defects  gradually 
diminishes. 

The  deformity  of  the  valves  is  brought  about  in  several  ways:  (1) 
Not  less  than  half  of  the  cases  are  the  direct  result  of  an  acute  endocarditis. 
In  discussing  the  etiology  of  acute  endocarditis  it  was  shown  that  acute 
rheumatic  fever  was  by  far  the  most  important  factor  leading  to  acute 
inflammatory  changes  in  the  valves  and  that  a  very  large  proportion  of 
these  acute  cases  terminated  in  chronic  valvular  defects.  Closely  allied 
to  the  rheumatic  cases  are  those  which  follow  chorea  and  tonsillitis.  Of 
the  other  acute  infectious  diseases,  any  one  of  them  may  cause  acute 
endocardial  changes  which  terminate  in  a  chronic  lesion,  although  the 
number  of  cases  having  their  origin  in  this  way  is  not  great.  In  a  not 
inconsiderable  number  of  cases,  particularly  when  the  mitral  valve  is 
involved,  no  etiological  factor  can  be  determined. 

2.  In  quite  a  large  number  of  cases  of  chronic  valvular  disease,  es- 
pecially in  those  past  the  middle  period  of  life,  we  are  unable  to  obtain 
a  history  of  acute  endocarditis.  In  these  cases  we  have  to  deal  with  a 
form  of   endocarditis   which  is   chronic  from  the  beginning.     Primary 

1  Jour.  Am.  Med.  Assoc,  October  2,  1915. 


ENDOCARDITIS  655 

chronic  endocarditis  is  caused  by  the  same  conditions  that  lead  to  general 
arterio-sclerosis.  Inasmuch  as  the  intimal  lining  of  the  arteries  and  the 
tissue  covering  the  valves  is  exactly  similar,  every  etiological  factor 
favorable  to  the  production  of  general  arterio-sclerosis  is  of  impor- 
tance in  the  etiology  of  chronic  valvular  disease.  Among  these  causes 
are  to  be  mentioned  the  general  wear  and  tear  incident  to  advan- 
cing years,  excessive  physical  labor,  overindulgence  in  food,  alcohol 
and  tobacco,  and  gout.  Chronic  interstitial  nephritis  is  also  frequently 
associated  with  primary  chronic  valvular  disease.  Whether  the  chronic 
valvulitis,  the  arterio-sclerosis  and  the  nephritis  are  due  to  the  same  cause 
or  one  arises  in  consequence  of  the  others,  is  not  clear.  It  is.  certain,  how- 
ever, that  two  or  all  three  of  these  conditions  frequently  occur  together. 

3.  Syphilis.- — -Within  the  past  decade  our  knowledge  regarding  the 
role  played  by  syphilis  in  the  causation  of  cardio-vascular  disease  has 
been  greatly  extended.  We  now  know  that  a  definite  group  of  cardiac 
cases  are  unmistakably  syphilitic  in  origin.  With  few  exceptions  the 
lesion  thus  far  proved  to  be  due  to  syphilis  is  aortic  insufficiency.  A  few 
instances  have  been  recorded  in  which  the  mitral  valve  was  the  site  of  a 
luetic  infection.  Doubtless  in  the  near  future  it  will  be  shown  that  all 
parts  of  the  heart  are  more  frequently  invaded  by  the  spirochseta  pallida 
than  is  at  present  believed  (see  p.  636). 

4.  Occasionally  a  chronic  valvular  lesion  is  detected  at  birth.  This 
may  be  due  to  congenital  malformation  or  a  fetal  endocarditis.  If  a 
congenital  anomaly  is  present  the  pulmonic  valve  is  the  one  commonly  at 
fault,  the  lesion  being  usually  a  stenosis  associated  with  some  other 
malformation  of  the  heart.  If  an  attack  of  fetal  endocarditis  has  occurred, 
the  valves  on  the  right  side  of  the  heart  are  most  commonly  involved. 

In  rare  instances  the  chronic  endocarditis  is  clue  to  a  rupture  of  one 
of  the  valve  segments.  The  aortic  leaflets  are  those  usually  torn  as  the 
result  of  some  severe  muscular  exertion. 

Cabot  has  recently  analyzed  600  cases  of  cardiac  disease  from  an 
etiological  standpoint.  Ninety-three  per  cent,  of  these  were  classified  in 
definite  groups  as  follows: 

Forty-five  per  cent,  were  rheumatic  in  origin.  Of  these  60  per  cent, 
occurred  in  women,  and  60  per  cent,  were  in  individuals  under  twenty-two 
years  of  age.  Twenty  per  cent,  had  a  nephritic  origin,  with  an  average  age 
of  thirty-six  years.  Fifteen  per  cent,  were  arteriosclerotic  in  nature,  with 
an  average  age  of  fifty-nine  years.  Twelve  per  cent,  were  due  to  syphilis, 
with  an  average  age  of  forty-seven  years,  70  per  cent  occurring  in  men. 
These  cases  were  comprised  of  aortic  insufficiency,  aneurism,  myocardi- 
tis; five  per  cent,  were  due  to  goitre. 

Morbid  Anatomy. — In  acute  endocarditis  the  physiological  defect 
produced  by  the  valvular  lesion  is  a  leakage  due  to  the  inability  of  the 
valves  to  properly  close  and  also  to  an  associated  myocarditis.  Obstruc- 
tion to  the  blood  current  does  not  occur  except  in  those  instances  of  malig- 
nant endocarditis  in  which  the  size  of  the  vegetations  partially  block  the 
mitral  or  aortic  rings.  In  the  chronic  form  of  endocarditis  the  lesion  may 
cause  obstruction  or  leakage  or  both. 

When  the  lesion  is  secondary  to  simple  acute  endocarditis  the  ultimate 
result  is  a  local  fibrosis  with  some  contraction  of  the  involved  area  of  the 
valve  segment  and  a  resulting  deformity. 

In  the  primary  form  of  chronic  endocarditis  the  valvular  changes, 


656  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

particularly  in  the  aortic  cusps,  are  identical  with  those  met  with  in 
arterio-sclerosis.  The  condition  is  non-inflammatory  and  is  dependent 
on  the  same  factors  which  lead  to  the  arterial  changes.  These  have  been 
alluded  to  already  in  discussing  the  etiology. 

The  end  result  in  both  instances  is  essentially  the  same.  The  con- 
nective tissue,  in  common  with  all  new  connective  tissue,  tends  to  undergo 
contraction.  This  may  curl  the  edges  of  the  valve  segments  or  produce 
shortening ;  in  either  case  a  leakage  results.  Or  the  edges  of  the  cusps  may 
undergo  fusion  along  their  opposed  edges;  later  as  they  become  stiff er  and 
more  rigid  a  stenosis  is  produced.  As  time  goes  on  degenerative  changes, 
calcification  and  atheromatous  ulceration  [may  develop  or  the  chorda? 
tendinese  may  undergo  thickening  and  constriction  and  thus  seriously 
interfere  with  the  proper  working  of  the  valve. 

In  many  cases  of  chronic  endocarditis  the  cardiac  damage  is  not  lim- 
ited to  the  valves.  The  lesions  not  infrequently  extend  to  the  adjacent 
areas.  Thus  in  aortic  lesions  the  first  part  of  the  aorta  may  be  affected 
with  sclerotic  changes  which  also  involve  the  orifices  of  the  coronary 
arteries.  In  this  way  myocardial  changes  may  be  brought  about  through 
interference  with  the  nutrition  of  the  heart.  "When  the  mitral  orifice  is 
involved  the  inflammatory  process  may  be  spread  into  the  heart  muscle 
surrounding  the  ring.  Owing  to  the  close  proximity  of  both  the  aortic 
and  mitral  valves  to  the  auriculo-ventricular  node  and  bundle,  serious 
disturbances  in  the  cardiac  rhythm  may  occur  if  the  inflammatory  process 
invades  the  muscular  tissue. 

Combined  Valvular  Lesions. — The  valvular  defect  may  be  single 
or  multiple.  Stenosis  is  often  accompanied  by  some  degree  of  leakage 
and  conversely  incompetence  may  be  associated  with  some  degree  of 
narrowing.  Furthermore,  two  or  more  valvular  orifices  are  frequently 
affected.  In  children  involvement  of  both  the  mitral  and  aortic  orifices  is 
not  uncommon  as  the  result  of  acute  rheumatic  fever.  Aortic  lesions  are 
more  commonly  uncombined  than  mitral  lesions.  This  is  to  be  explained 
by  the  fact  that  syphilis  is  so  frequently  the  etiological  factor  in  aortic 
insufficiency.  Secondary  involvement  of  the  tricuspid  orifice  is  a  common 
event  in  mitral  disease. 

Generally  speaking  two  or  more  valvular  defects  are  more  serious 
than  a  single  lesion  but  at  times  the  ill  effects  of  regurgitation  may  be 
offset  by  a  certain  degree  of  stenosis. 

The  morbid  anatomy  will  be  considered  in  greater  detail  when  we  take 
up  the  individual  lesions. 

Pathological  Physiology  of  Chronic  Valvular  Lesions. — The  normal 
heart  performs  its  work  with  a  regularity  and  precision  which  amply 
justifies  Krehl's  statement  that  it  is  the  best  motor  known  to  man. 
" Sixty  times  a  minute  at  least;  3600  times  an  hour;  86,400  times  per  day, 
for  us  heedful  and  heedless,  does  this  shuttle  of  life  flit  to  and  fro;  for  us 
in  tireless  periods  this  pendulum  of  man's  gravitation  tells  the  seconds 
which  will  never  return ' '  ( Allbutt) . 

Not  only  does  it  proceed  smoothly  and  rhythmically  in  the  perform- 
ance of  its  work  when  the  body  is  at  complete  rest  but  it  also  possesses 
the  power  of  adapting  itself  to  the  varying  demands  made  upon  it. 
Within  reasonable  limits  the  healthy  heart  rarely  fails  in  any  effort. 
This  does  not  necessarily  mean  that  every  healthy  heart  is  capable  of  per- 
forming the  same  amount  of  work  or  possesses  the  same  power  of  meeting 


ENDOCARDITIS  657 

sudden  emergencies.  It  is  to  be  borne  in  mind  that  the  heart  muscle  is 
subject  to  the  same  general  laws  as  the  skeletal  muscles.  The  stronger 
and  the  better-nourished  the  general  musculature,  the  more  apt  is  the 
heart  to  be  correspondingly  strong,  and  the  more  capable  of  meeting  any 
sudden  demand  that  may  be  made  upon  it.  This  relationship  which 
exists  between  the  cardiac  muscle  and  the  skeletal  muscles  explains  why 
the  individual  who  has  undergone  a  course  of  physical  training  or  has 
become  used  to  hard  physical  labor  can  take  part  in  athletic  contests  or 
swing  a  heavy  sledge  hammer  without  producing  exhaustion.  On  the 
other  hand,  the  man  who  leads  a  sedentary  life  and  whose  muscles,  as  a 
consequence,  become  soft  and  flabby  will  certainly  have  a  heart  muscle 
correspondingly  reduced  in  its  capacity  for  meeting  any  unusual  strain. 
Before  such  an  individual  can  hope  to  do  anything  requiring  exertion  to 
which  he  is  unaccustomed,  the  muscles  must  be  exercised  and  hardened 
and  this  applies  quite  as  much  to  the  cardiac  as  to  the  voluntary  muscles. 

As  a  result  of  exercise  the  heart  may  become  more  or  less  hyper- 
trophied  without  any  injurious  results;  providing,  of  course,  this  is 
brought  about  gradually.  That  the  strength  of  the  heart  has  a  great- 
deal  to  do  with  feats  of  strength  or  endurance  is  borne  out  by  the  fact 
that  the  most  successful  athletes  possess  hearts  of  good  size  and  a 
functional  capacity  above  the  ordinary  It  has  long  been  known  that 
race  horses  possess  relatively  large  hearts. 

The  adaptability  of  the  heart  to  cope  with  the  various  emergencies 
it  is  required  to  meet  is  also  seen  in  the  manner  in  which  it  overcomes 
these  demands.  "For  example,  when  a  ventricle  in  diastole  becomes 
unusually  filled  (even  up  to  six  times  its  customary  capacity) ,  then  with 
the  next  systole,  it  drives  out  not  all  the  blood,  perhaps,  but  at  least  several 
times  the  ordinary  quantity.  On  the  other  hand,  if  the  arterial  resist- 
ance be  suddenly  increased,  it  is  as  promptly  overcome  by  the  succeeding 
ventricular  contractions.  There  is  no  time  lost  in  experimentation. 
The  demand  and  the  accomplishment  occur  together"  (Krehl). 

Were  it  not  for  this  ability  of  the  heart  to  adjust  itself  to  changed 
conditions  which  may  either  gradually  or  suddenly  thrust  themselves 
upon  it  the  individual  who  becomes  the  subject  of  a  chronic  valvular  lesion 
would  quickly  succumb. 

The  heart  valves  perform  two  functions:  (1)  They  direct  the  blood 
current  in  the  proper  direction.  (2)  They  prevent  leakage  by  tightly 
closing  the  openings.  This  is  accomplished  by  the  apposition  of  the 
valve  segments  which  are  controlled  by  the  papillary  muscles  and  chor- 
da? tendinese  and  also  by  the  contraction  of  the  ring  of  muscle  surround- 
ing the  opening.  During  systole  the  orifices  become  smaller  while  during 
diastole  they  are  relatively  too  large  for  the  valves. 

Now,  when  it  comes  to  pass  that  the  valves  become  deformed  as 
the  result  of  a  chronic  endocarditis,  the  heart  is  confronted  with  addi- 
tional work.  Either  it  must  overcome  the  resistance  caused  by  stenosis 
of  one  of  the  orifices  or  it  must  properly  empty  an  abnormally  distended 
cavity  caused  by  leakage.  Under  normal  conditions  in  a  given  interval, 
as  much  blood  is  driven  out  of  the  heart  as  flows  into  it.  If,  therefore, 
in  the  presence  of  a  valvular  defect,  the  heart  were  to  work  with  the  same 
energy  as  under  normal  conditions,  an  impairment  of  circulation  would 
soon  arise  which  would  quickly  lead  to  a  fatal  termination.  Fortunately 
the  heart  is  possessed  of  a  reserve  force  which  enables  it  to  compensate 


658  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

for  these  defects  and  to  so  carry  on  its  work  that  no  circulatory  ill  effects 
are  felt.  When  a  heart  is  damaged  by  a  valvular  defect  and  at  the  same 
time  does  its  work  as  efficiently  as  a  normal  heart,  we  speak  of  the  lesion 
as  a  compensated  one.  The  period  of  compensation  is  variable;  it 
may  last  throughout  life.  In  the  majority  of  instances,  however,  the 
compensation  is  only  relative  and  the  patient  will  remain  free  from 
subjective  symptoms  only  as  long  as  care  is  taken  to  spare  the  heart  in 
every  way.  Thus  in  some  individuals  varying  amounts  of  exercise 
may  be  permissible  while  in  others  the  circulatory  equilibrium  is  main- 
tained only  when  the  patient  is  kept  at  complete  rest.  Compensation 
depends  on  three  factors,  namely:  the  extent  of  the  valvular  damage; 
the  demands  which  may  be  made  upon  the  heart  either  through  exertion 
or  through  some  acute  intercurrent  illness;  and,  lastly,  the  degree 
of  hypertrophy  which  takes  place.  Hypertrophy  of  the  heart,  arising 
as  the  result  of  valvular  disease,  is  variable  in  degree.  It  may  be  enor- 
mous as  in  cases  of  aortic  insufficiency,  or  it  may  be  very  slight  as  in 
many  cases  of  mitral  insufficiency.  This  hypertrophy  does  not  affect 
all  the  chambers  of  the  heart  uniformly  but  is  more  noticeable  in  those 
portions  in  which  the  valvular  defect  has  led  to  increased  functional 
activity. 

In  the  majority  of  cases  with  a  well-marked  valvular  lesion  there  comes 
a  time  when  the  heart  begins  to  falter  and  is  no  longer  able  to  accomplish 
the  additional  work  demanded  of  it.  The  failure  of  the  heart  to  carry 
on  the  burden  may  be  due  to  the  fact  that  the  valvular  defect  gradually 
increases  or  it  may  be  that  the  continued  strain  eventually  leads  to 
exhaustion  of  the  cardiac  muscle.  In  still  other  instances  the  heart  is 
thrown  out  of  its  stride  by  some  acute  intercurrent  illness  which  in- 
directly affects  it.  So  long  as  the  compensation  is  adequate,  symptoms 
indicative  of  heart  disease  are  absent.  At  first  the  symptoms  may  be 
trifling  but  they  are  apt  to  become  worse  either  gradually  or  suddenly. 
When  this  condition  of  affairs  arises  it  is  spoken  of  as  failing  or  broken 
compensation  or  decompensation. 

Valvular  defects  of  the  heart  are  recognized  clinically  mainly  by  the 
presence  of  murmurs  but  it  must  not  be  assumed  that  the  absence  of 
a  murmur  is  positive  evidence  that  a  valvular  lesion  is  not  present.  Great 
widening  of  an  orifice  may  be  present  and  permit  of  the  regurgitation 
of  large  quantities  of  blood  without  producing  a  murmur.  In  cases  of 
stenosis  of  the  mitral  orifice  it  not  infrequently  happens  that  the  murmur 
will  disappear  and  yet  a  diagnosis  of  mitral  stenosis  can  be  made,  with 
a  fair  degree  of  certainty,  from  the  presence  of  other  physical  signs. 

Regurgitant  murmurs,  as  a  rule,  lack  the  rasping  quality  common 
to  those  associated  with  an  obstructive  lesion. 

A  soft  blowing  murmur  may  indicate  that  the  valvular  damage  is 
slight  or  it  may  be  significant  of  an  enfeebled  muscle.  The  distinction 
is  usually  readily  made  from  a  consideration  of  the  associated  signs  and 
symptoms.  Thus,  if  there  are  no  symptoms  or  signs  of  beginning  cardiac 
failure,  one  is  safe  in  assuming  that  the  valvular  damage  is  slight ;  con- 
versely, a  feeble  murmur  associated  with  such  symptoms  indicates 
serious  valvular  damage  or  an  associated  myocardial  degeneration. 

A  loud  murmur  is  usually  indicative  of  good  compensation  and  points 
to  a  strong,  healthy  heart  muscle.  A  change  in  the  intensity  of  the 
murmur  is  very  significant.     If  it  is  noted  that  a  murmur  is  gradually 


ENDOCARDITIS  659 

becoming  less  intense  it  is  a  fair  assumption  that  the  heart  muscle  is  be- 
ginning to  weaken  and  this  is  often  the  forerunner  of  failing  compensa- 
tion. In  such  cases  the  murmur  or  murmurs  may  disappear  entirely. 
If,  as  a  result  of  rest  and  cardiac  medication,  the  circulatory  equilibrium 
is  reestablished  the  murmur  begins  to  return,  at  first  feebly,  and  as  the 
heart  tends  to  recovery  the  murmur  becomes  louder  and  louder.  In 
exceptional  instances  the  murmur  is  so  loud  that  it  may  be  heard  at 
some  distance  from  the  chest  wall;  musical  murmurs  are  not  infrequently 
of  this  character. 

The  duration  of  the  murmur  is  also  of  importance.  If  it  occupies 
but  a  portion  of  the  systole  or  diastole  the  presumption  is  that  the 
damage  is  slight  while  the  entire  replacement  of  the  first  or  second  sound 
by  a  murmur  is  indicative  of  an  extensive  lesion  and  one  in  which  com- 
pensation will  be  maintained  with  some  difficulty. 

It  is  of  the  utmost  importance  to  bear  in  mind  that  the  murmur  is, 
for  the  most  part,  of  relatively  little  consequence.  This  has  been  em- 
phasized by  Osier,  who  states  that  for  those  who  are  not  adept  in  aus- 
cultation the  best  judgment  of  the  condition  of  the  heart  may  be  gathered 
from  inspection  and  palpation.  With  an  apex  beat  in  the  normal 
situation  and  a  regular  rhythm  the  auscultation  phenomena  may  be 
practically  disregarded.  The  most  important  consideration  in  valvular 
disease  is  the  condition  of  the  heart  muscle.  So  long  as  the  lesion  is 
well  compensated  and  the  heart  performs  its  work  with  practically  the 
same  efficiency  as  a  normal  heart  there  is  nothing  to  be  done  except 
guard  the  patient  against  overexertion,  or  anything  that  will  unduly 
increase  the  cardiac  work.  If,  on  the  other  hand,  cardiac  symptoms 
gradually  develop  it  is  highly  probable  that  the  heart  muscle  is  beginning 
to  fail.  The  compensation  may  be  broken  in  one  or  two  ways.  First, 
there  may  arise  an  exhaustion  of  the  heart  muscle  which  is  brought  about 
by  continued  overwork  in  the  attempt  to  overcome  the  valvular  defect 
or  some  extra  strain  may  be  imposed  upon  the  heart  which  it  is  unable 
to  meet.  Second,  the  mechanism  which  governs  the  cardiac  rhythm 
may  be  disturbed  and  any  of  the  abnormal  rhythms  may  occur.  Heart 
block,  auricular  fibrillation  and  extrasystoles  are  all  apt  to  add  to  the 
st lain  of  a  heart  already  taxed  to  its  limit.  The  character  of  the  various 
types  of  arrhythmia  and  the  means  employed  for  their  recognition  are 
discussed  in  full  in  Chap.  XV. 

Symptoms. — Irrespective  of  the  valve  involved  or  whether  the  lesion 
has  produced  obstruction,  or  leakage,  or  both,  the  symptoms  which 
arise  as  the  result  of  valvular  disease  are  with  a  few  minor  exceptions 
essentially  the  same.  In  mitral  lesions  pulmonary  congestion  is  a  more 
marked  feature  than  in  the  aortic  cases  and  cyanosis  is  common.  Chil- 
dren who  are  the  subjects  of  chronic  valvular  disease  are  commonly 
anemic  and  undersized.  In  aortic  insufficiency  true  angina  or  anginoid 
attacks  of  pain  occur  more  frequently  than  in  other  forms  of  valvular 
disease,  pallor  of  the  face  i-  common,  and  vertigo  and  mental  symptoms 
are  often  very  pronounced. 

Shortness  of  breath  is  common  to  all  forms  of  valvular  disease  and 
is  present,  at  some  stage  of  the  trouble,  in  the  great  majority  of  cases. 
Prior  to  the  stage1  of  broken  compensation  it  occurs  only  after  some  un- 
usual exertion;  the  degree  of  exertion  necessary  to  cause  shortness  of 
breath   varies    greatly  in  the  individual  case.     When    the  heart  fails, 


660  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

true  dyspnea  or  orthopnea  is  common.  In  some  instances  patients 
are  suddenly  seized  with  paroxysmal  attacks  of  dyspnea.  These  attacks 
are  often  not  associated  with  exertion  and  not  uncommonly  occur  at 
night.     Cheyne-Stokes  breathing  often  occurs  in  cardiac  cases. 

Aside  from  attacks  of  true  angina  or  seizures  resembling  it,  and  which 
occur,  for  the  most  part,  in  aortic  insufficiency,  actual  pain  is  not  com- 
mon as  a  result  of  valvular  lesions.  Precordial  distress  and  a  sense  of 
substernal  oppression  are,  however,  quite  common.  Not  infrequently 
the  sense  of  oppression  is  referred  to  the  epigastric  region.     Very  often 


Fig.  380. — General  edema  occurring  in  broken  compensation.  Mitral  and  tricuspid 
insufficiency  complicated  by  serofibrinous  pericarditis.  The  cardiac  dulness  is  enormously 
enlarged,  especially  to  the  left,  the  apex  beat  is  displaced  downward  and  outward.  The 
scrotum  and  lower  extremities  are  edematous,  the  hands  and  face  cyanotic,  the  liver  en- 
larged^ tender  and  pulsating.  The  cross-hatched  area  indicates  the  location  of  the  to-and- 
fro  pericardial  friction.  The  dotted  regions  indicate  the  areas  and  direction  of  transmission 
of  the  mitral  and  tricuspid  systolic  murmurs.  The  case  is  of  rheumatic  origin  and  the  phys- 
ical signs  are  shown  as  they  occurred  during  the  second  attack  of  broken  compensation. 

the  precordial  distress  is  associated  with  an  annoying  palpitation  and 
throbbing.  Chest  pain  in  cardiac  cases  may  be  due  also  to  a  pulmonary 
infarct. 

Edema  is  another  very  common  manifestation  of  cardiac  disease. 
It  differs  from  the  edema  occurring  in  Bright 's  disease,  in  that  it  first 
manifests  itself  in  the  lower  extremities  and  is  much  more  noticeable 
in  the  evening  after  the  patient  has  been  up  and  about  all  day.  After 
a  night's  rest  the  edema  may  disappear  by  morning.  As  the  heart 
muscle  becomes  weaker,  the  edema  not  only  persists  but  is  apt  to  increase. 
The  lower  extremities  become  water-logged  and  in  males  the  scrotum  and 


ENDOCARDITIS  661 

penis  may  become  tremendously  edematous  (Fig.  380).  In  extreme 
cases  some  one  or  all  of  the  serous  cavities  may  contain  fluid.  Hydro- 
thorax  is  relatively  common  (see  section  on  "  Hydrothorax  ") . 

Gastro-intestinal  symptoms  are  often  marked.  A  not  inconsiderable 
number  of  cases  of  failing  compensation  come  to  the  hospital  complain- 
ing of  nausea  and  vomiting  and  it  not  infrequently  happens  that  they 
have  been  treated  outside  for  some  stomach  disorder.  This  can  occur 
only  as  a  result  of  carelessness  as  the  most  superficial  examination  will 
reveal  the  fact  that  the  heart  is  at  fault.  This  condition  of  affairs  is 
brought  about  by  tricuspid  insufficiency  which  results  in  the  damming 
back  of  the  blood  in  the  venous  system,  thus  producing  congestion  of 
the  liver  and  the  gastro-intestinal  mucosa.  In  extreme  cases  the  liver 
becomes  greatly  engorged,  very  painful  and  may  pulsate.  Another 
condition  sometimes  produced  by  the  hepatic  congestion  and  gastro- 
intestinal catarrh  is  jaundice. 

Cardiac  cases  quite  commonly  suffer  from  transient  attacks  of  faint- 
ness  and  dizziness.  Sleeplessness  or  sleep  that  is  frequently  broken 
is  often  a  very  annoying  condition.  In  some  patients,  particularly  those 
suffering  from  aortic  insufficiency,  hallucinations,  delusions  or  a  suicidal 
tendency  are  not  infrequently  encountered.  Hemiplegia,  or  some  other 
gross  cerebral  lesion,  may  occur  as  a  result  of  an  embolus. 

Having  reviewed  the  general  aspects  of  valvular  diseases  we  will  now 
consider  the  individual  lesions  more  in  detail. 

MITRAL  INSUFFICIENCY 

Etiology. — This  is  one  of  the  most  common,  if  not  the  commonest, 
of  cardiac  lesions.  A  leakage  at  the  mitral  orifice  may  arise  under  the 
following  conditions:  (1)  The  most  frequent  cause  of  mitral  insufficiency 
is  acute  endocarditis  occurring  in  young  people.  In  the  majority  of  in- 
stances the  endocarditis  has  resulted  from  an  attack  of  acute  rheumatic 
fever,  chorea  or  tonsillitis.  Although  these  conditions  are  the  chief 
offenders,  any  one  of  the  acute  infectious  diseases  may  produce  the  condi- 
tion. I  have  already  emphasized  the  fact  that  in  the  so-called  rheu- 
matic endocarditis  it  is  the  mitral  valve  which  is  principally  involved. 
(2)  In  a  second  group  composed,  for  the  most  part,  of  individuals 
who  have  passed  the  fifth  or  sixth  decade  of  life,  the  leakage  is  caused 
by  a  chronic  sclerosis  of  the  valve.  This  is  a  part  of  a  general  arterio- 
sclerosis and  occurs  without  an  antecedent  history  of  acute  endocarditis. 
Varying  degrees  of  sclerosis  of  the  mitral  valve  are  encountered  in  nearly 
all  people  of  advanced  years  and  just  as  in  the  case  of  the  arteries,  it 
is  indicative  of  the  general  wear  and  tear  of  work.  (3)  Occurring  with 
even  greater  frequency  is  the  leakage  which  occurs  as  the  result  of 
relative  insufficiency.  In  this  group  the  trouble  is  muscular  and  not 
valvular.  The  valve  itself  is  healthy  but  owing  to  lack  of  tonicity  or 
as  the  result  of  acute  or  chronic  myocarditis  the  left  ventricle  dilates 
and  in  so  doing  stretches  the  mitral  ring.  Thus  while  the  valve  under 
normal  conditions  is  capable  of  closing  the  auriculo-ventricular  opening, 
coaptation  of  its  edges  is  prevented  by  the  distended  ring.  Relative 
or  muscular  insufficiency  may  occur  in  a  variety  of  conditions.  It  is 
a  frequent  finding  in  the  aneimas,  in  the  acute  feveis,  notably  typhoid, 
and  in  conditions  characterized  by  exhaustion  such  as  Graves '  disease, 


662 


DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


neurasthenia,  etc.  Relative  insufficiency  of  the  mitral  valve  is  also 
of  common  occurrence  in  other  forms  of  valvulitis  when  compensation 
begins  to  fail.  (4)  Regurgitation  may  result  from  rupture  of  the  valve 
or  one  of  the  chordae  tendineae.     This  accident  is  very  rare. 

Morbid  Anatomy . — In  considering  lesions  involving  the  mitral  valve 
it  is  to  be  borne  in  mind  that  neither  the  mitral  nor  tricuspid  valve  pos- 
sesses distinct  cusps  as  in  the  case  of  the  aortic  and  pulmonic  valves. 


Fig.  381. — Chronic  mitral  endocarditis.      The  mitral  valve  is  thickened  along  its  free  edges, 
the  leaflets  are  slightly  retracted,  and  the  chorda?  tendinea?  are  distinctly  shortened. 


Both  the  mitral  and  tricuspid  valves  consist  of  a  veil  or  curtain  which 
hangs  in  the  ventricular  cavity  and  is  continuous  around  its  whole  cir- 
cumference. Although  these  valves  are  commonly  spoken  of  as  having 
an  anterior  and  a  posterior  leaflet,  no  such  division  actually  exists. 

When  chronic  endocarditis  of  the  mitral  valve  succeeds  the  acute  form 
of  the  disease,  it  is  usually  slow  in  forming.  The  newly  formed  connect- 
ive tissue  within  the  substance  of  the  valve  gradually  shrinks,  causing 
both  a  shortening  of  the  valve  and  a  curling  up  of  its  free  edges  (see 


ENDOCARDITIS  663 


Fig.  381).  In  other  instances  the  free  edges  of  the  valve  are  drawn 
together,  thus  producing  some  narrowing  of  the  orifice  as  well  as  in- 
sufficiency. Along  the  free  edges  of  the  valve  the  tissue  may  be  car- 
tilaginous in  character  and  in  addition  the  chordae  tendineae  are  short- 
ened,  sclerotic  and    often    fused    together.     While    in    most    instances 


nWH    Y    7-  wl  lnsuffic}eQcy.     Showing    very    extensive    tissue    destruction      The 

tt  "^  at  *he  central  part,  of  the  valvular  margin  have  been  destroyed  ulcera- 

tion leaving  only  short  shriveled  stumps.  A  few  verrucose  vegetations  are  seen  The 
ventricular  wall  is  much  thickened.     {Specimen  from  the  Pennsylvania  Hospital) 

chronic  rheumatic  endocarditis  is  gradual  in  its  evolution,  there  are 
instances  in  which  the  process  is  very  rapid  in  its  progress  In  still 
other  instances  the  acute  stage  is  very  destructive,  causing  widespread 
erosion  m  both  the  valve  and  the  chordae  tenclineaa  and  causing  within 
a  few  days  an  extensive  leak  (see  Fig.  382). 


664  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

In  the  primary  sclerotic  type  the  process  is  identical  with  what  we 
encounter  in  arterio-sclerosis.  It  is  non-inflammatory  in  character  and 
as  time  goes  on  the  fibrous  changes  become  more  and  more  marked. 
Later,  salts  are  deposited  in  the  valve  and  in  extreme  cases  both  the  valve 
and  ring  may  form  a  rigid  membrane.  The  chordae  tendinese  may  be 
involved,  also  becoming  both  thickened  and  contracted.  In  some  in- 
stances the  contraction  is  so  marked  that  the  valves  seem  to  be  inserted 
upon  the  apices  of  the  papillary  muscles.  Some  degree  of  stenosis  is 
commonly  associated  with  the  insufficiency. 

Emboli  sometimes  occur  in  mitral  insufficiency.  They  may  arise 
from  a  thrombus  in  the  left  auricle  or  from  fresh  vegetations  on  the  valve. 
Occasionally  venous  thromboses  are  met  with. 

Pathological  Physiology. — When  leakage  occurs  at  the  left  auriculo- 
ventricular  opening,  a  part  of  the  contents  of  the  left  ventricle  is 
thrown  back  into  the  auricle  during  systole.  This  increases  the  amount 
of  blood  the  left  auricle  is  forced  to  accommodate.  As  a  result  the  auricle 
becomes  dilated  and  hypertrophied;  damming  back  of  the  blood  takes 
place  in  the  pulmonary  circulation,  which  results  in  raising  the  blood- 
pressure  and  this  in  turn  increases  the  work  of  the  right  ventricle.  The 
increased  work  thrust  upon  the  right  ventricle  causes  it  to  hypertrophy 
and  just  as  in  the  case  of  mitral  stenosis,  the  circulatory  equilibrium 
will  be  maintained  just  so  long  as  the  right  ventricle  can,  without  undue 
effort,  overcome  the  resistance  in  the  pulmonary  circulation.  If,  how- 
ever, the  leakage  at  the  left  auriculo-ventricular  orifice  increases  to  a 
point  where  the  right  ventricle  is  no  longer  able  to  maintain  the  pressure 
in  the  pulmonary  circulation,  compensation  fails. 

Some  degree  of  hypertrophy  and  dilatation  of  the  left  ventricle  always 
exist  in  cases  of  mitral  insufficiency.  During  ventricular  diastole  the 
blood  flows  from  the  auricle  into  the  ventricle  with  greater  force  than 
normal  owing  to  the  increased  pressure  in  the  pulmonary  veins.  In 
addition  the  amount  that  flows  into  the  ventricle  must  be  greater  than  nor- 
mal if  the  body  is  to  receive  the  proper  amount  of  blood.  The  increased 
pressure  with  which  the  blood  flows  plus  the  increased  amount  both  lead 
to  dilatation  or  an  increase  in  the  capacity  of  the  left  ventricle. 

Hypertrophy  is  brought  about  by  reason  of  the  fact  that  the  left 
ventricle  during  each  systole  is  forced  to  expel  a  greater  amount  of  blood 
than  normal.  The  greater  amount  is  driven  into  the  aorta  and  a  very 
much  smaller  amount  escapes  back  into  the  auricle.  The  amount  that 
regurgitates  will  of  course  depend  on  the  size  of  the  leak  and  determine  the 
amount  of  hypertrophy  necessary  to  compensate  for  the  damage. 

As  we  have  already  pointed  out,  however,  it  is  the  right  ventricle 
which  really  controls  the  situation.  Failure  of  compensation  is  brought 
about  either  by  an  increase  of  the  mitral  leak  or  from  changes  in  the 
muscle  of  the  right  ventricle.  When  the  right  ventricle  is  no  longer  able 
to  carry  on  the  burden  relative  insufficiency  of  the  tricuspid  orifice  occurs, 
the  right  auricle  becomes  dilated,  and  the  blood  is  dammed  back  into  the 
large  venous  trunks.  This  results  in  an  engorgement  of  the  entire  venous 
system  which  produces  cyanosis,  edema  and  passive  congestion  of  the 
viscera,  notably  the  liver  (see  "Tricuspid  Insufficiency,"  p.  685). 

Symptoms. — If  the  leak  is  small  and  the  compensation  is  adequate, 
no  symptoms  will  be  present  even  with  moderate  exertion.  In  other 
cases  the  compensation  may  be  good  unless  some  unusual  strain  is  put  upon 


ENDOCARDITIS  665 

the  heart.  In  such  cases  undue  exertion  may  produce  shortness  of  breath 
and  precordial  pain  or  oppression.  In  long-standing  cases  in  which  the 
compensation  falls  just  short  of  being  complete,  shortness  of  breath 
occurs  on  the  slightest  exertion,  there  is  a  bluish  tint  of  the  lips,  the 
fingers  may  be  clubbed  and  recurring  hydrothorax,  usually  on  the  right 
side,  may  occur.  Patients  suffering  from  chronic  mitral  disease  are  es- 
pecially liable  to  attacks  of  bronchitis  during  the  winter. 

As  time  goes  on  and  compensation  gradually  fails,  the  dyspnea  and 
cyanosis  become  more  and  more  marked,  slight  edema  of  the  legs  may 
be  noted  at  night  and  there  are  evidences  of  congestion  of  the  lungs.  The 
pulmonary  changes  are  never  as  marked  as  in  cases  of  mitral  stenosis. 
The  tendency  is  rather  to  congestions  and  edema  of  the  bases  of  the  lungs 
rather  than  the  chronic  fibrous  changes  sometimes  noted  in  association 
with  obstruction  of  the  mitral  orifice.  Hemoptysis,  although  not  as 
frequent  as  in  cases  of  mitral  stenosis,  often  occurs. 

Compensation  may  fail  gradually  or  it  may  be  precipitated  abruptly 
as  the  result  of  some  unusual  exertion,  mental  shock  or  an  intercurrent 
acute  illness. 

Broken  compensation  is  characterized  by  distressing  palpitation  of  the 
heart,  attacks  of  precordial  oppression,  extreme  cyanosis  and  attacks 
of  dyspnea  or  orthopnea  which  may  occur  in  paroxysms  and  result  from 
pulmonary  congestion  or  edema.  The  patient  is  restless  and  sleep 
is  often  broken  accompanied  by  nightmare,  or  by  attacks  of  cardiac 
oppression.  For  a  more  detailed  description  the  reader  is  referred  to  the 
section  on  "Tricuspid  Insufficiency." 

Even  a  very  severe  attack  of  broken  compensation  may  be  recovered 
from  and  the  patient  may  remain  well  for  years,  but  as  a  rule,  once  the 
circulatory  equilibrium  is  broken  there  is  apt  to  be  a  recurrence  of  the 
attacks. 

Physical  Signs. — Inspection. — If  compensation  is  well  maintained, 
the  patient  presents  the  appearance  of  good  health.  Depending  on  the 
degree  of  failure  of  compensation  there  will  be  noted  some  cyanosis  of 
the  face,  edema  of  the  lower  extremities  and  difficulty  in  breathing. 

In  children  if  the  heart  is  much  hypertrophied  the  cardiac  region  may 
be  slightly  bulged  forward.  The  apex  beat  is  displaced  to  the  left 
and  sometimes  downward  into  the  sixth  interspace.  In  long-stand- 
ing cases  the  apex  beat  may  be  as  far  to  the  left  as  the  mid-axillary 
line.  Extension  of  the  cardiac  impulse  to  the  left  is  brought  about 
partly  by  the  enlarged  left  ventricle  and  partly  by  the  hypertrophied 
right  ventricle.  The  former  tends  to  carry  the  apex  downward  while 
the  latter  pushes  the  apex  outward  to  the  left.  In  compensated  cases 
the  impulse  is  not  diffuse  and  is  much  stronger  than  normally.  If 
compensation  fails,  the  cardiac  impulse  is  very  diffuse  and  modulatory 
in  appearance. 

Hypertrophy  of  the  heart  as  the  result  of  the  mitral  regurgitation 
is  usually  associated  with  the  rheumatic  group  of  cases.  In  elderly 
people  suffering  from  the  arterio-sclerotic  type  of  the  disease  the  apex 
beat  may  be  in  its  normal  position  and  hypertrophy  of  the  left  ventricle 
is  very  slight. 

Marked  pulsation  in  the  epigastric  region,  due  to  hypertrophy  of 
the  right  ventricle,  is  often  marked.  Unless  the  leak  is  very  slight,  some 
enlargement  of  the  veins  at  the  root  of  the  neck  is  usually  present. 


666  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

When  compensation  fails,  these  veins  may  become  enormously  enlarged 
and  pulsate  with  each  systole. 

Palpation.— This  serves  to  indicate  the  strength  and  character  of  the 
impulse.  In  not  a  few  cases  there  is  felt  a  systolic  thrill  which  ex- 
tends as  far  to  the  left  as  the  axilla.  The  shock  of  the  second  sound 
may  also  be  felt. 

The  impulse  in  mitral  insufficiency  is  normal  in  well  compensated 
cases  and  the  blood-pressure  is  about  normal.  If  there  is  an  associated 
kidney  lesion  the  pulse  often  feels  hard  and  the  blood-pressure  may  be 
distinctly  higher  than  normal. 

According  to  Broadbent  it  is  a  safe  working  hypothesis  to  assume 
that  a  mitral  murmur  is  not  attended  with  serious  regurgitation  while  the 
pulse  remains  normal.  While  marked  irregularity  of  the  pulse  is  often 
the  precursor  of  a  fatal  termination,  irregularity  of  the  heart's  action 
may  occur  early  and  is  not  inconsistent  with  good  compensation  and 
fair  health  for  a  period  of  years. 

The  irregularity  of  the  pulse  in  mitral  disease  is  generally  due  to 
auricular  fibrillation  or  extrasytoles,  and  is  very  characteristic.  The 
varying  size  of  the  pulse  waves  is  extremely  striking.  The  ventricular 
contractions  remain  coordinate,  but  their  rhythm  is  disturbed  and  the 
beats  are  very  irregular,  being  now  large  and  now  small,  although  the 
pulse  periods  are  nearly  equal  (see  Figs.  143  and  153). 

Percussion. — The  area  of  cardiac  dulness  is  increased  and  this  in- 
crease may  in  extreme  cases  be  tremendous.  Not  only  is  the  left  border 
of  cardiac  dulness  extended  far  beyond  the  normal  limits,  but  it  also  may 
extend  to  or  beyond  the  right  parasternal  line.  The  upper  limit  may  be 
at  the  second  rib  (see  Fig.  172). 

Auscultation. — The  recognition  of  mitral  insufficiency  depends  largely 
on  the  presence  of  a  systolic  murmur  heard  at  or  above  the  apex  and  trans- 
mitted toward  the  axilla.  The  sound  produced  by  the  backward  escape 
of  the  blood  is  subject  to  many  variations.  There  may  be  nothing- 
more  than  a  roughening  of  the  first  sound.  If  an  actual  murmur  is  present, 
it  may  be  rasping  and  loud  with,  at  times,  a  musical  quality.  In  other 
instances  it  is  soft  and  low-pitched.  The  murmur  may  be  of  short  dura- 
tion or  it  may  occupy  the  entire  systolic  period.  A  noticeable  feature 
of  the  murmur  is  that  it  diminishes  in  intensity  in  contrast  to  the  cres- 
cendo murmur  of  mitral  stenosis.  The  murmur  may  be  transmitted 
but  a  short  distance  to  the  left,  but  in  well-marked  cases  the  sound  is 
nearly  always  propagated  to  the  axilla  and  is  often  heard  in  the  left  inter- 
scapular region  (see  Figs.  199  and  200).  When  loud,  it  may  be  heard  over 
the  entire  chest,  and  in  such  cases  the  question  often  arises  as  to  whether 
the  murmur  is  single  and  has  its  origin  at  the  mitral  or  aortic  orifice 
or  whether  there  is  a  double  murmur  present.  If  the  murmur  at  the 
apex  diminishes  in  intensity  as  the  base  of  the  heart  is  approached  but 
has  the  same  duration  and  tone,  it  is  caused  by  mitral  insufficiency 
alone.  If,  however,  the  murmur  diminishes  and  then  increases  in  in- 
tensity as  the  aortic  area  is  reached  and  in  addition  is  of  shorter  or 
longer  duration  and  differs  in  tone,  there  is  a  strong  probability  that  two 
distinct  murmurs  are  present.  In  cases  of  mitral  insufficiency  the  sec- 
ond pulmonic  sound  is  sharply  accentuated  and  often  reduplicated. 

Generally  speaking,  a  loud  murmur  implies  strength  of  contraction 
and  indicates  good  compensation.     On  the  other  hand,  a  short,  faint 


ENDOCARDITIS  667 

murmur  which  varies  in  intensity  and  duration  in  successive  beats 
indicates  a  weak  muscle.  If  in  a  case  under  constant  observation  it 
is  noted  that  the  murmur  is  gradually  becoming  less  intense,  one  should 
be  suspicious  of  failing  compensation.  And  conversely  the  first  evidence 
pointing  to  restored  compensation  may  be  the  return  of  the  murmur 
or  the  gradual  increase  in  intensity  of  a  previously  feeble  murmur. 

With  an  actual  leak  at  the  mitral  orifice  it  is  not  always  easy  to  deter- 
mine whether  the  insufficiency  is  due  to  an  organic  lesion  of  the  valves 
or  to  relative  insufficiency  due  to  myocarditis,  the  anemias  or  some  toxe- 
mia. As  a  rule  the  murmur  of  relative  insufficiency  is  less  intense  and 
is  apt  to  disappear  or  become  more  marked  with  change  of  posture. 
Thus  it  may  be  heard  in  the  recumbent  and  not  in  the  erect  position. 
Furthermore,  if  the  murmur  is  associated  with  anemia  or  some  acute 
infection,  the   murmur  disappears  as  the  general    condition   improves. 

Oille,  Graham  and  Detweiller1  have  expressed  the  belief  that  pul- 
monary systolic  murmurs  so  frequently  heard  in  "run  down"  and 
anemic  individuals  are  not  functional  but  are  indicative,  in  many  in- 
stances, of  mitral  regurgitation. 

A  not  infrequent  source  of  error  is  the  presence  of  a  cardiorespiratory 
murmur.  This  murmur  is  relatively  common  and,  while  heard  more  often 
and  more  distinctly  about  the  apex  and  to  the  left  of  the  heart,  should 
cause  no  confusion  if  attention  is  paid  to  the  time  of  its  occurrence 
(see  also  p.  247).  A  cardio-respiratory  murmur  consists  of  several  short 
whiffs  occurring  during  ventricular  systole. 

Diagnosis. — The  diagnosis  of  mitral  insufficiency  is,  in  the  majority 
of  cases,  not  difficult,  although  it  is  not  always  easy  to  determine  whether 
the  murmur  is  due  to  an  organic  lesion  or  to  relative  insufficiency. 
The  organic  lesion  usually  has  the  following  characteristics:  The  apex 
beat  is  displaced  to  the  left;  there  is  a  systolic  murmur  heard  best  at  the 
apex  and  transmitted  to  the  left,  and  an  accentuated  second  pulmonic 
sound. 

In  the  presence  of  anemia  or  during  convalescence  from  some  acute 
illness  the  occurrence  of  a  mitral  murmur  is  probably  indicative  of  relative 
insufficiency  and  a  lack  of  muscle  tone.  A  murmur  of  relative  insuffi- 
ciency may  also  develop  in  the  hypertrophied  heart  associated  with 
Bright's  disease  or  general  arterio-sclerosis.  Unless  some  such  condition 
is  present  an  apical  systolic  murmur  had  better  be  regarded  as  indicating- 
some  valvular  damage.  The  significance  of  these  murmurs  is  fully  appre- 
ciated by  insurance  companies.  Except  in  rare  instances  individuals 
having  a  systolic  murmur  at  the  apex  are  rejected  as  experience  has 
shown  that  in  the  great  majority  of  cases  they  are  bad  risks. 

MITRAL  STENOSIS 

In  estimating  the  relative  frequency  of  the  different  valvular  defects 
mitral  regurgitation  occupies  the  first  place.  Most  observers  place  mitral 
stenosis  and  aortic  regurgitation  second.  MacKenzie,  on  the  other  hand, 
has  expressed  the  belief  that  mitral  stenosis  is  the  most  common  of 
valvular  defects  with  which  heart  failure  is  associated. 

Etiology. — This  lesion  is  encountered  more  frequently  among  females 
than  males.     This  may  be  ascribed  to  the  fact  that  acute  rheumatic 

1  Jour.  Am.  Med.  Assoc,  October  2,  1915. 


668  DISEASES    OF   THE    PERICARDIUM,    HEART,    AND    AORTA 

fever,  chorea  and :  tonsillitis  prevail  more  in  girls  than  in  boys  and  also 
because  in  both  these  diseases  the  endocarditis  more  often  affects  the 
mitral  valve.  Acute  rheumatic  fever  is  credited  with  being  the  etiological 
factor  in  from  one-half  to  two-thirds  of  the  cases.  In  not  a  few  cases  of 
mitral  stenosis  it  is  not  possible  to  obtain  a  definite  history  of  any  etiolog- 
ical factor.  In  the  great  majority  of  cases,  however,  the  stenosis  is  the 
direct  consequence  of  one  or  more  attacks  of  acute  rheumatic  endocarditis. 
Very  often  the  stenosis  develops  in  chronic  endocarditis  as  a  sequel  to 
a  previous  insufficiency.  In  such  cases  the  valve  becomes  more  and  more 
sclerotic  until  finally  the  signs  of  obstruction  overshadow  those  of  regurgi- 
tation. Chronic  interstitial  nephritis  is  not  uncommonly  associated 
with  this  type  of  the  disease,  the  valvular  lesion  having  apparently  an 
arterio-sclerotic  basis.  A  few  cases  have  been  reported  in- which  the 
stenosis  apparently  followed  a  severe  blow  on  the  chest.  Experimentally 
hemorrhagic  extravasation  into  the  pericardium  and  endocardium  can 
be  produced  by  blows  inflicted  upon  the  precordium. 

Morbid  Anatomy. — As  the  result  of  an  attack  of  acute  endocarditis, 
changes  are  produced  in  the  valve  itself,  in  the  chordae  tendinese,  or  in 
both.  This  lesion  is  never  recognized  during  the  course  of  the  acute 
process  which  produces  it.  It  is  only  later  when  cicatrization  is  es- 
tablished and  narrowing  of  the  mitral  orifice  is  produced  that  the  charac- 
teristic features  of  the  condition  appear.  While  in  many  cases  the  initial 
damage  does  not  spread,  the  tendency  of  the  scar  tissue  is  to  extend,  thus 
making  the  valve  defect  progressively  worse.  The  initial  stage  is  similar 
to  that  seen  in  mitral  insufficiency.  When  the  free  edges  of  the  valvular 
curtain  are  chiefly  concerned,  the  deformity  usually  assumes  the 
well-known  funnel-shaped  orifice  (see  Fig.  383).  This  is  the  type  of 
defect  which  is  generally  seen  in  early  life  as  the  result  of  a  rheumatic 
infection.  On  the  other  hand,  the  "button-hole"  form  of  stenosis  is  ob- 
served with  far  greater  frequency  in  adults  (see  Fig.  202) .  In  this  type  the 
whole  valve  becomes  thickened  as  the  result  of  an  overgrowth  of  fibrous 
tissue.  This  scar  tissue  eventually  leads  to  puckering  and  thickening  so 
that  the  valve  is  converted  into  a  transverse  septum  or  diaphragm  with  a 
narrow  slit  between  the  auricle  and  ventricle.  The  opening  may  be  still 
further  narrowed  by  verrucose  vegetations  (see  Fig.  389).  In  addition 
the  chordae  tendineae  are  often  thickened  and  matted  together  and  the 
papillary  muscles  markedly  fibroid  in  character.  One  of  the  most  serious 
effects  produced  by  mitral  lesions  is  disturbance  of  the  cardiac  rhythm 
Owing  to  the  close  proximity  of  the  mitral  valve  to  the  auriculo-ventricu- 
lar  bundle  this  specialized  muscle  often  becomes  the  site  of  degenerative 
changes.  As  a  result,  heart  block,  auricular  fibrillation  and  extrasystoles 
may  develop. 

There  is  some  difference  of  opinion  as  to  whether  pure  stenosis  without 
insufficiency  ever  occurs.  In  view  of  the  character  of  the  lesion  it  can 
easily  be  understood,  however,  that  some  leakage  is  inevitable  in  many 
of  the  cases,  although  the  clinical  evidence  of  this  may  be  masked  by  the 
more  pronounced  signs  of  the  stenosis. 

Although  there  is  usually  some  evidence  of  hypertrophy  of  the  left 
ventricle  it  is  not  apt  to  be  marked  unless  a  considerable  degree  of  in- 
sufficiency is  present  also.  The  chamber  which  bears  the  brunt  of  the 
attack  is  the  left  auricle  which  may  become  enormously  distended. 
Backward  pressure  in  the  pulmonary  circulation  leads  to  pulmonary 


ENDOCARDITIS 


669 


congestion  and  finally  to  hypertrophy  and  dilatation  of  the  right  ventricle. 
Thrombi,  free  or  attached  to  the  auricular  wall,  may  form  as  the  result  of 
stasis,  and  from  these  emboli  may  be  swept  off,  thus  adding  to  the  gravity 
of  the  situation  (see  Fig.  384). 


F 1 1 ; .  8s:-i.  Mitral  stenosis.  Mitral  orifice  was  not  incised;  its  leaflets  are  enormously 
thickened  and  contracted,  showing  at  the  right  junction  slight  calcification;  the  whole  pre- 
senting the  appearance  of  the  funnel-shaped  buttonhole  mitral.  The  chordae  tendinese 
are  enormously  thickened,  retracted  and  adherent,  and  are  attached  to  papillary  muscles 
which  are  much  elongated  and  have  sclerotic  tips.  The  fibrosis  of  the  anterior  mitral 
leaflet  extends  forward  along  the  septum,  below  the  bases  of  the  aortic  valves,  producing 
a  thickening  which  extends  transversely  through  the  bundle  of  His.  The  ventricular 
cavity  is  enlarged. 

Pathological  Physiology. — Although  the  ultimate  results  are  similar 
when  compensation  fails,  the  problem  of  maintaining  the  circulatory 
equilibrium  in  mitral  stenosis  is  somewhat  different  from  that  in  eases 
of  insufficiency.     In  the  former  the  difficulty  lies  in  filling  the  left  ven- 


670  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

tricle  and,  from  the  very  beginning,  in  overcoming  the  stasis  in  the  pul- 
monary circulation;  in  the  latter  the  important  factor  is  the  emptying  of 
the  left  ventricle  and  it  is  not  until  the  leakage  assumes  serious  propor- 
tions that  disturbance  in  the  pulmonary  circulation  becomes  a  menace. 


Fig  384.— Ball  thrombus  in  the  left  auricle.  A  large,  dark,  ball-shaped  thrombus  lies 
free  in  the  left  auricular  cavity.  Numerous  smaller  mural  thrombi  are  seen  enmeshed  in 
the  columnar  carries  and  chords  tendines.  The  left  ventricular  wall  which  is  elsewhere 
hypertrophied,  is  noticeably  thinned  near  the  apex.     (Photograph  by  Dr.  Alfred  K.  Alien.) 

The  effect  of  obstruction  at  the  mitral  orifice  first  manifests  itself  in 
the  left  auricle,  the  wall  of  which  becomes  slightly  hypertrophied.  In- 
asmuch as  the  capability  of  the  left  auricle  to  hypertrophy  is  limited, 


ENDOCARDITIS  671 

this  chamber  sooner  or  later  dilates.  (See  Fig.  198).  Even  prior  to 
this  it  is  unable  to  entirely  empty  itself  and  as  a  result  the  blood  is 
dammed  back  into  the  pulmonary  circulation.  This  in  turn  increases 
the  work  of  the  right  ventricle  which  hypertrophies  in  order  to  over- 
come the  increased  resistance  in  the  pulmonary  vessels.  Just  as  in 
mitral  insufficiency  the  key  to  the  situation  is  the  ability  of  the  right 
ventricle  to  overcome  the  resistance  in  the  pulmonary  circulation. 
Forced  to  maintain  the  pressure  in  the  pulmonary  vessels,  the  right 
ventricle  dilates  and  this  in  turn  eventually  leads  to  dilatation  of 
the  right  auricle  with  damming  back  of  the  blood  in  the  systemic 
veins  as  the  result  of  tricuspid  insufficiency.  In  mitral  stenosis  leakage 
from  the  veins  into  the  peritoneal  cavity  is  often  a  marked  feature.  This 
results  from  secondary,  relative,  tricuspid  insufficiency.  The  failure  of 
the  right  ventricle  also  leads  to  stasis  in  the  pulmonary  circulation  which 
manifests  itself  by  the  symptoms  and  signs  of  hydrothorax  or  passive 
congestion.  In  long-standing  cases  the  stasis  of  the  blood  in  the  pulmo- 
nary vessels  may  lead  to  the  deposition  of  blood  pigment.  As  a  result, 
the  lung  becomes  of  a  reddish-brown  color.  In  addition,  there  is  an 
overgrowth  of  fibrous  tissue  imparting  to  the  lung  a  tough,  inelastic 
feel.     The  condition  is  known  as  brown  induration  of  the  lung. 

An  occasional  effect  of  distention  of  the  left  auricle  is  pressure  on  the 
left  recurrent  laryngeal  nerve.  Fetterolf  and  Norris1  have  collected 
37  instances.  Their  explanation  is,  that  such  distention  by  dilatation 
of,  and  upward  pressure  on,  the  left  pulmonary  artery  may  cause  left  re- 
current laryngeal  paralysis  by  compression  of  this  nerve  between  the 
last-named  vessel  and  the  aortic  arch. 

Symptoms. — The  fact  that  mitral  stenosis  is  so  frequently  the  fore- 
runner of  serious  cardiac  failure  has  given  the  impression  that  it  is  always 
followed  by  evil  results.  Quite  the  contrary  is  the  case,  however.  There 
are  many  individuals  in  whom  mitral  stenosis  exists  in  a  latent  form  and 
in  whom  the  discovery  of  its  presence  is  made  accidentally.  On  the 
other  hand,  a  well-marked  mitral  stenosis  is  often  the  cause  of  cardiac 
symptoms  which  are  ascribed  to  other- lesions.  In  a  study  of  200  autop- 
sied  cases  of  mitral  stenosis  Cabot2  states  that  the  condition  was  over- 
looked in  53  per  cent. 

A  patient  with  well-marked  physical  signs  may  be  entirely  free  from 
symptoms  or  at  the  most  suffer  from  slight  dyspnea  on  exertion.  Breath- 
lessness  is  perhaps  the  earliest  manifestation  and  with  it  there  is  often 
a  slight  cyanotic  tinge  of  the  lips.  An  appearance  of  ruddy  health  is 
often  present,  due  to  the  congestion  of  the  fine  capillaries  over  the  cheek 
bones.  When  the  lesion  develops  in  adults  it  is  often  well  borne  for  an 
indefinite  period.  In  the  type  which  arises  as  the  result  of  an  attack 
of  acute  rheumatic  fever  in  children  the  symptoms  are  usually  marked 
and  become  progressively  worse.  Children  subject  to  this  lesion  are 
often  delicate  looking,  undersized,  and  are  especially  liable  to  secondary 
at  lacks  of  endocarditis  (see  Fig.  15). 

Pulmonary  attacks  may  develop  before  compensation  is  seriously 
interfered  with.  Thus  as  the  result  of  fibroid  changes  in  the  lungs  (brown 
induration)  the  patient  may  have  cough  and  expectoration.  The  sputum 
at  this  stage  of  the  trouble  may  be  blood-streaked  from  time  to  time. 

1  Am.  Jour.  Med.  Sc,  May,  1911. 

2  Trans.  Assoc.  Am.  Phys.,  1914. 


672  DISEASES    OF   THE    PERICARDIUM,    HEART,    AND    AORTA 

Under  the  circumstances  the  blood  is  the  result  of  the  high  pressure 
in  the  pulmonic  vessels  which  causes  the  rupture  of  the  capillaries. 
Individuals  suffering  from  mitral  stenosis  are  extremely  liable  to  attacks 
of  bronchitis  at  which  time  blood-streaked  sputum  is  especially  apt  to 
occur.  What  has  been  described  as  a  pseudo-tuberculous  type  of 
mitral  stenosis  is  not  infrequently  seen  in  young  women.  Such  individuals 
are  pale,  underweight,  and  are  subject  to  frequent  attacks  of  bronchitis 
which  is  often  attended  with  blood-streaked  sputum,  especially  at  the 
menstrual  periods.  When  compensation  fails,  bloody  sputum  or  even 
small  hemoptyses  very  commonly  occur  as  the  result  of  pulmonary  in- 
farcts. In  a  few  cases  the  voice  is  husky  or  the  cough  is  brassy  in  char- 
acter as  the  result  of  paralysis  of  the  left  recurrent  laryngeal  nerve. 

Precordial  pain  and  tenderness  are  often  complained  of.  Riesman 
states  that  in  young  girls  complaining  of  precordial  pain,  the  possibility  of 
mitral  stenosis  should  always  be  borne  in  mind.  It  is  a  common  lesion, 
especially  among  the  Russian  Jewish  population,  and  is  often  overlooked. 
Pain  may  be  present  also  in  the  epigastrium  as  the  result  of  engorgement 
of  the  liver.  A  sense  of  oppression  in  the  precordium  and  attacks  of 
tachycardia  or  palpitation  are  often  annoying  symptoms.  Embolic 
phenomena  are  encountered  more  often  in  this  form  of  valvular  disease 
than  any  other.  The  emboli  may  arise  from  a  secondary  vegetative 
endocarditis  but  are  more  often  due  to  thrombi  in  the  left  auricle  or  pul- 
monary vessels.  Pulmonary  infarcts  are  common.  A  not  infrequent 
accident  is  the  occurrence  of  hemiplegia  due  to  an  embolism;  and  this 
may  be  the  first  indication  of  the  presence  of  the  cardiac  lesion. 

When  compensation  finally  fails,  the  evidences  of  venous  stasis  be- 
come marked.  There  is  no  essential  difference  between  the  phenomena 
which  arise  as  the  result  of  failing  compensation  in  mitral  stenosis  and 
those  occurring  in  mitral  insufficiency,  save  in  one  particular.  In  the 
latter  the  venous  stasis  results  in  marked  subcutaneous  edema  while 
in  mitral  stenosis  an  excessive  amount  of  peritoneal  fluid  may  appear 
before  edema  of  the  legs  and  may  persist  after  the  latter  disappears. 
In  addition  engorgement  of  the  liver  is  more  evident  in  cases  of  obstruc- 
tion. In  many  of  the  fatal  cases  fever  and  other  evidences  of  an  acute 
infection  are  frequently  present. 

Physical  Signs. — Inspection  may  show  nothing  abnormal.  In  children 
the  precordium  may  bulge  forward  and  marked  pulsation  may  be  seen 
in  the  interspaces  to  the  left  of  the  sternum.  In  adults  the  apex  beat  may 
occupy  its  normal  position  or  be  displaced  slightly  to  the  left.  This 
may  be  due  to  hypertrophy  of  the  left  ventricle,  or  to  dilatation  and  hy- 
pertrophy of  the  right  ventricle.  In  the  later  stages  of  the  disease,  when 
dilatation  of  the  heart  has  taken  place,  the  cardiac  impulse  may  be  wavy 
and  diffuse.  Pulsation  may  be  seen  to  the  right  of  the  sternum  and  also 
in  the  epigastrium.  In  cases  in  which  hoarseness  is  present,  direct  inspec- 
tion of  the  larynx  will  usually  show  paralysis  of  the  left  vocal  cord. 

Palpation. — In  many  cases  of  mitral  stenosis  during  the  stage  of 
compensation,  the  diagnosis  may  be  made  by  palpation  alone.  This  is 
possible  through  the  detection  of  a  presystolic  thrill  felt  slightly  above  and 
to  the  right  of  the  apex  beat.  If  the  hand  is  placed  over  this  portion 
of  the  precordium,  there  is  imparted  to  it  a  fine  vibration  which  occurs 
during  all  or  a  portion  of  the  diastole  and  terminates  in  the  abrupt, 
sharp  shock  of  the  first  sound.     The  thrill  may  not  be  present  constant!}' 


ENDOCARDITIS  673 

in  the  same  case.  In  some  instances  it  is  best  felt  during  expiration: 
in  others,  it  is  brought  out  by  slight  exertion;  while  in  still  other  cases 
it  may  be  detected  by  altering  the  posture  of  the  patient.  The  presys- 
tolic thrill  may  precede  the  appearance  of  the  pres3^stolic  murmur  b}r 
several  years  (Mackenzie).  In  addition  to  feeling  the  shock  of  the  first 
sound  at  the  apex  there  may  be  present  also  a  distinct  shock  accompany- 
ing the  second  sound  at  the  pulmonic  area. 

In  the  later  stages  of  the  disease  when  the  compensation  becomes 
broken,  the  thrill  usually  disappears.  A  pres3^stolic  thrill  may  occur  also 
in  association  with  Flint's  murmur.  The  differentiation  of  Flint's  mur- 
mur from  that  of  the  mitral  stenosis  will  be  considered  under  "  Diagnosis. " 

Palpation  confirms  inspection  as  regards  the  character  of  the  cardiac 
impulse. 

The  pulse  at  the  wrist  is  usually  small.  The  blood- pressure  as  a 
rule  varies  but  slightly  from  the  normal,  but  the  pulse  pressure  is  often 
diminished.  The  most  interesting  feature  connected  with  the  pulse  is 
the  irregularity  which  develops  during  the  later  stages  of  the  disease  and, 
in  some  instances,  when  compensation  is  well  maintained.  Auricular 
fibrillation  is  especially  apt  to  develop  in  cases  of  mitral  stenosis.  It 
gives  rise  to  a  form  of  arrhythmia  characterized  by  marked  irregularity 
in  both  the  force  and  rhythm  of  the  pulse  beats  (see  Figs.  143  and  153). 
Although  auricular  fibrillation  is  always  to  be  looked  upon  as  of  serious 
import  it  does  not  necessarily  mean  immediate  danger;  it  may  persist 
for  years. 

Percussion. — In  the  region  of  the  apex,  cardiac  dulness  may  extend 
farther  to  the  left  than  normal  in  case  there  is  much  hypertrophy  of  the 
left  ventricle.  At  the  base,  dulness  is  apt  to  extend  higher  and  farther  to 
the  left  than  is  ordinarily  the  case  owing  to  dilatation  of  the  conus  arteri- 
osus; dilatation  of  the  pulmonary  artery  may  be  a  factor  also.  Usually 
cardiac  dulness  extends  slightly  beyond  the  right  border  of  the  sternum,  as 
the  right  auricle  is  hypertrophied  or  dilated.  When  compensation  fails, 
dulness  to  the  right  of  the  sternum  may  be  marked.  Enlargement  of  the 
cardiac  dulness  upward  and  to  the  left  is  due  to  dilatation  of  the  left 
auricular  appendage.  This  rarely  if  ever  occurs  in  simple  mitral  insuf- 
ficiency (see  Fig.  183). 

Auscultation. — The  auscultatory  signs  in  mitral  stenosis  are  often 
extremely  perplexing,  especially  to  the  beginner.  In  many  cases  we  have 
three  sounds  to  deal  with  instead  of  two,  as  in  other  valvular  lesions.  In 
addition  the  character  of  the  murmur  varies  according  to  the  stage  of  the 
disease.  It  is  important  to  bear  in  mind  that  the  lesion  which  leads  to 
stenosis  is  a  progressive  one  and  for  this  reason  both  the  signs  and  the 
symptoms  will  vary  in  different  cases  and  in  the  same  case  from  time  to 
time. 

There  are  several  murmurs  occurring  in  cases  of  mitral  stenosis.  With 
one  exception  they  are  heard  over  a  small,  circumscribed  area  a  little  to 
the  right  of  the  apex  beat  and  have  a  very  limited  range  of  transmission. 
The  most  characteristic  sign  of  mitral  stenosis,  and  the  first  of  the  mur- 
murs to  appear,  is  the  presystolic  murmur.  This  murmur  is  sharply 
localized,  the  punctum  maximum  being  at  or  a  little  to  the  right  of  the 
apex  beat  (see  Fig.  201).  It  occurs  late  in  the  diastolic  period  and  is 
rumbling,  rough  or  vibratory  in  character.  It  is  usually  of  brief  duration 
and  precedes  or  runs  up  to  the  first  sound.     In  some  instances  the  dura- 

43 


674  DISEASES    OF   THE    PERICARDIUM,    HEART,    AND   AORTA 

tion  is  relatively  long  and  may  occupy  a  greater  portion  of  the  diastolic 
period.  Another  distinctive  feature  of  the  presystolic  murmur  is  that 
it  is  crescendo  in  character.  The  pitch  and  intensity  of  the  sound  rises 
rapidly  and  abruptly  terminates  with  the  loud  snap  of  the  first  sound, 
although  occasionally  there  is  a  brief  interval  between  the  cessation  of  the 
murmur  and  the  first  sound.  The  murmur  is  often  accompanied  by  a 
presystolic  thrill.  The  presystolic  murmur  is  usually  present  in  well- 
compensated  cases  of  mitral  stenosis.  Its  genesis  has  already  been  dis- 
cussed. In  the  later  stages  of  the  disease,  when  the  auricle  becomes 
paralyzed  and  auricular  fibrillation  sets  in,  the  murmur  disappears. 

Of  almost  equal  importance  is  the  character  of  the  first  sound.  This 
occurs  immediately  after  the  presystolic  murmur.  It  is  very  loud,  of 
short  duration,  sharply  accentuated  and  closely  resembles  an  accentuated 
second  sound.  It  is,  indeed,  often  mistaken  for  the  later,  especially  by  the 
beginner.  The  third  factor  is  the  second  sound  at  the  apex.  Thus  we 
have  occurring  in  close  succession  the  presystolic  murmur,  the  accentu- 
ated first  sound  and  the  normal  second  sound.  It  is  to  be  remembered, 
however,  that  the  second  sound  at  the  pulmonic  area  is  usually  accentu- 
ated as  the  result  of  the  increased  pressure  in  the  pulmonary  vessels  and 
in  addition  it  may  be  reduplicated. 

As  the  stenosis  increases  another  murmur,  diastolic  in  time,  appears. 
According  to  Mackenzie  this  murmur  is  limited  to  the  area  about  the  apex. 
It  begins  immediately  after  the  second  sound  and  while  at  first  faint  and 
inconstant  it  gradually  becomes  more  pronounced.  This  murmur  at 
first  occupies  the  first  portion  of  the  diastolic  period  and  is  diminuendo  in 
character.  It  may,  however,  merge  into  the  presystolic,  thus  producing 
a  continuous  murmur  throughout  diastole.  It  is  loud  in  the  beginning, 
then  diminishes  in  intensity  and  finally  ends  in  the  crescendo  presystolic 
portion.  With  failure  of  the  left  auricle  the  presystolic  portion  disap- 
pears and  the  diastolic  portion  may  remain,  occupying  a  portion  or  all  of 
diastole.  This  diastolic  murmur  is  produced  by  the  accumulation  of 
blood  in  the  auricle  during  the  ventricular  systole.  It  begins  with  the 
opening  of  the  mitral  valves  at  a  time  when  the  ventricular  pressure  is 
below  that  of  the  auricle. 

Another  diastolic  murmur  commonly  heard  in  cases  of  mitral  stenosis 
is  one  which  is  heard  along  the  left  border  of  the  sternum.  This  murmur, 
sometimes  known  as  the  Graham  Steele  murmur,  is  ascribed  to  incom- 
petence of  the  pulmonary  valves  as  the  result  of  the  high  pressure  in  the 
pulmonary  artery.  It  closely  resembles  the  soft  blowing  murmur  asso- 
ciated with  aortic  regurgitation.  In  22  out  of  50  autopsied  cases  in  which 
this  murmur  was  present  Cabot1  was  unable  to  demonstrate  disease  of  the 
pulmonary  valves,  dilatation  of  the  pulmonary  artery  or  any  evidence  of 
aortic  incompetence. 

Finally  there  may  be  associated  with  these  presystolic  and  diastolic 
murmurs  a  short,  soft,  systolic  murmur  at  the  apex.  This  murmur  is 
probably  due,  in  most  instances,  to  the  presence  of  slight  incompetence. 
Mackenzie,  however,  states  that  it  differs  from  the  murmur  of  true  regur- 
gitation in  that  it  begins  a  short  interval  after  the  first  sound,  rises  in 
intensity  and  terminates  in  the  second  sound. 

The  untangling  of  the  numerous  sounds  heard  in  the  region  of  the 
apex  in  cases  of  mitral  stenosis  is  usually  a  perplexing  task  for  the  begin- 
1  Trans.  Assoc.  Am.  Phys.,  191-4. 


ENDOCARDITIS  675 

ner.  Inasmuch  as  the  auscultatory  phenomena  are  confined  to  the  region 
of  the  apex,  it  is  usually  possible  to  find  a  point  at  the  base  of  the  heart 
where  the  two  cardiac  sounds  are  unmistakable.  By  gradually  approach- 
ing the  apex,  it  can  usually  be  determined  in  what  respect  they  change  or 
whether  additional  sounds  develop. 

It  has  already  been  pointed  out  that  the  lesion  of  mitral  stenosis  is  a 
progressive  one  and  that  for  this  reason  the  signs  and  symptoms  show 
corresponding  changes.  Broadbent  has  made  a  useful  clinical  division  to 
indicate  these  changes.  He  recognizes  three  stages:  (1)  That  of  good 
compensation  in  which  the  presystolic  murmur,  the  snapping  first  sound 
and  the  second  sound  are  plainly  audible  at  the  apex.  A  diastolic  mur- 
mur may  appear  in  this  period.  (2)  The  presystolic  murmur  persists,  but 
is  associated  with  a  diastolic  murmur,  the  first  sound  is  even  more  accentu- 
ated, and,  of  extreme  diagnostic  importance,  the  second  sound  at  the 
apex  disappears.  It  is  in  this  stage  that  errors  are  most  apt  to  occur,  as 
the  long  continuous  diastolic  and  presystolic  murmur  and  the  accen- 
tuated first  sound  may  be  mistaken  for  a  systolic  murmur  and  accentu- 
ated second  sound.  Dyspnea,  hemoptysis  and  other  evidences  of  stasis 
in  the  pulmonaiy  circulation  are  often  present  in  this  stage.  (3)  The 
pres3rstolic  murmur  and  thrill  have  disappeared  but  a  short  diastolic 
murmur  may  persist.  The  second  sound  is  inaudible  and  all  that  may 
remain  of  the  auscultatory  signs  is  the  sharply  accentuated  first  sound. 
Auricular  fibrillation,  as  manifested  by  marked  irregularity  of  the 
pulse  and  more  or  less  disappearance  of  the  murmurs,  is  common  dur- 
ing this  stage.  The  evidences  of  stasis  in  the  pulmonary  circulation  be- 
come increasingly  evident.  To  these  three  stages  Hirschfelder  has 
added  a  fourth  in  which  there  are  present  all  the  manifestations  of  broken 
compensation. 

Diagnosis. — The  diagnosis  of  mitral  stenosis  in  the  stage  of  compensa- 
tion offers  no  serious  difficulties,  as  the  presence  of  the  presystolic  thrill 
and  murmur  and  the^rmpping  first  sound  are_guite_distinctiye.  The  real 
clifficulty~occurs  in  the  second  and  especially  the  third  stage,  when  the 
characteristic  auscultatory  features  have  disappeared.  In  such  cases  the 
snapping  firs^sound,  and  the  presence  of  auricular  fibrillation,  even  in  the 
absence  of  cardiac  murmurs,  should  arouse  one's  suspicious  that  the  cause 
of  the  cardiac  failure  is  mitral  stenosis.  Patients  admitted  to  hospitals 
in  the  last  stages  of  broken  compensation  offer  the  greatest  diagnostic 
difficulty. 

Flint's  Murmur. — The  association  of  this  murmur  with  aortic  incom- 
petence and  the  mechanism  of  its  production  have  been  considered  (see 
pp.  244  and  680 J.  Like  the  murmur  of  mitral  obstruction  it  is  presystolic 
in  time  and  heard  at  or  near  the  apex  of  the  heart.  Thayer1  found  Flint's 
murmur  present  in  33  of  58  cases  of  aortic  insufficiency  and  Phear2  has  re- 
ported 46  cases  in  which  there  was  a  pres3^stolic  apical  murmur  without 
initial  stenosis;  in  17 instances  there  was  aortic  incompetence;  in  20  adher- 
ent pericardium ;  in  the  remainder  there  was  no  valve  lesion  but  in  some  of 
these  t  here  was  dilatation  of  the  left  ventricle.  The  Flint  murmur  is  dis- 
tinguished from  the  presystolic  murmur  due  to  mitral  stenosis  by  the 
following  points:  It  is  never  as  loud  and  rasping  in  character  and  is  not 
associated  with  the  accentuated  first  sound.     In  mitral  stenosis  the  sys- 

1  Trans.  Assoc.  Am.  Phys.,  1901. 
-  Lancet,  1S95,  ii,  716. 


676  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

tolic  shock  of  the  first  sound  can  be  felt  while  in  the  case  of  Flint's  mur- 
mur the  cardiac  impulse  is  diffuse  and  heaving.  In  addition  Flint's  mur- 
mur is  associated  with  the  arterial  phenomena  seen  in  aortic  regurgitation. 

Tuberculosis. — Strange  as  it  may  seem  a  diagnosis  of  tuberculosis 
instead  of  mitral  obstruction  is  not  uncommon.  As  a  rule  it  is  to  be 
ascribed  to  carelessness.  Although  there  are  cough,  expectoration,  at 
times  blood-streaked  sputum,  sometimes  fever,  a  rapid  pulse  and  the 
presence  of  rales  in  the  lungs  in  both  conditions,  careful  examination  of 
the  heart  will  usually  give  the  correct  clue  as  to  the  origin  of  the  symp- 
toms. Among  2113  cases  seen  at  the  Phipps  Institute  there  occurred  13 
instances  of  mitral  stenosis  and  9  more  in  which  there  was  a  double  mitral 
lesion.  Stenosis  of  the  mitral  orifice  and  pulmonary  tuberculosis  may 
occur  in  the  same  individual. 

Aneurism. — Reference  has  been  made  to  the  fact  that  in  some  in- 
stances distention  of  the  left  auricle  may  cause  'paralysis  of  the  left  recur- 
rent laryngeal  nerve.  In  such  cases  there  is  hoarseness,  a  brassy  cough, 
and  paralysis  of  the  left  vocal  cord.  Under  these  circumstances  a  diag- 
nosis of  aneurism  of  the  arch  of  the  aorta  may  be  made.  The  ausculta- 
tory phenomena  at  the  apex  should  serve  to  distinguish  them.  In  case 
there  is  any  doubt,  the  X-rays  will  easily  differentiate  the  two  conditions. 

AORTIC  INSUFFICIENCY 

Clinically  this  is  the  most  interesting  of  the  valvular  lesions.  It 
causes  very  distinct  alterations  in  the  physics  of  the  circulation  and,  even 
when  combined  with  other  valvular  lesions,  dominates  the  picture. 

Etiology. — This  lesion  is  encountered  most  frequently  in  males  of 
middle  age  or  those  approaching  this  period.  There  may  be  an  antece- 
dent history  of  acute  rheumatic  fever,  syphilis,  pneumonia,  severe  exertion 
or  alcoholism.  Although  rheumatic  fever  is  a  frequent  cause  it  does  not 
attack  the  aortic  leaflets  with  anything  like  the  frequency  that  it  does  the 
mitral  valve.  Rheumatic  endocarditis  affecting  the  aortic  valve  is 
usually  seen  in  children  (see  Fig.  194).  The  importance  of  syphilis  is 
becoming  more  and  more  apparent  and  a  very  large  number  of  the  cases 
seen  among  those  in  young  adult  life  are  due  to  this  cause  (see  Fig.  190). 
A  considerable  number  of  infants  dying  soon  after  birth  also  have  been 
found  to  have  spirochetae  in  the  aorta.  The  part  played  by  syphilis  in 
the  production  of  changes  involving  the  first  part  of  the  aorta  and  the 
aortic  ring  has  been  fully  discussed  elsewhere  (see  p.  718). 

Muscular  strain  is  a  well-recognized  factor.  In  not  a  few  cases  there 
is  no  obvious  cause,  the  lesion  being  a  part  of  a  general  sclerotic  process 
such  as  occurs  in  those  of  advancing  years.  In  rare  instances  aortic  in- 
sufficiency is  due  to  a  rupture  of  one  of  the  valve  segments  as  the  result  of 
severe  muscular  exertion  or  it  may  be  due  to  a  congenital  deformity. 

Morbid  Anatomy. — The  scar  tissue  which  develops  in  the  valve  seg- 
ments, whether  it  is  produced  by  an  acute  inflammatory  process,  syphilis 
or  a  chronic  sclerotic  change,  tends  to  shrink  and  produce  deformity. 
The  free  edges  of  the  segments  may  be  curled  back  or  as  a  result  of  re- 
traction the  free  edges  fail  to  come  into  complete  apposition  and  thus  fail 
to  close  the  orifice.  Sometimes  one  of  the  segments  becomes  perforated 
during  the  acute  stage  or  a  rupture  occurs  later  as  the  result  of  strain. 
As  a  consequence  of  the  leak  thus  produced,  a  part  of  the  blood  regurgi- 


ENDOCAEDITIS  677 

tates  from  the  aorta  back  into  the  left  ventricle  during  diastole.  The 
amount  of  blood  which  escapes  backward  will  depend  on  the  size  of  the 
opening  left  by  the  improper  closure  of  the  valves  and  by  the  tonus  of 
the  heart  muscle. 

If  the  opening  is  instantly  made  as  the  result  of  rupture  of  one  of  the 
segments  a  fatal  result  may  be  produced  as  the  heart  cannot  accommodate 
itself  to  the  sudden  strain.  In  the  usual  type  of  case  the  opening  is  gradu- 
ally formed  and  the  heart  is  able  to  adapt  itself  to  the  increased  work 
demanded  of  it.  The  chief  burden  falls  upon  the  left  ventricle  which 
often  becomes  enormously  hypertrophied.  The  heart  of  aortic  insuffi- 
ciency is  one  of  the  largest  met  with  and  is  often  referred  to  as  the  cor 
bovinum  (see  Figs.  181  and  193).  Great  hypertrophy  of  the  heart,  how- 
ever, is  not  a  constant  accompaniment  of  aortic  insufficiency  as  the 
opening  may  be  very  slight  and  the  amount  of  blood  which  regurgitates 
small. 

Relative  insufficiency  of  the  aortic  valve  rarely  occurs  as  the  result 
of  cardiac  dilatation  but  a  permanent  stretching  of  the  aortic  ring  is 
not  infrequent  secondarily  to  syphilitic  aortitis.  In  this  case  the  valve 
segments  themselves  are  intact  but  the  leakage  is  produced  by  the  in- 
ability of  the  valve  to  close  the  enlarged  opening. 

Disease  of  the  first  part  of  the  aorta  is  also  apt  to  involve  the  ori- 
fices of  the  coronary  arteries  and  thus  cause  attacks  of  true  angina. 
Even  without  involvement  of  the  coronary  openings  the  circulation  in  the 
coronary  arteries  may  be  embarrassed  as  a  result  of  the  lowering  of  the 
pressure  in  the  aorta  due  to  the  backward  leak. 

In  most  cases  of  aortic  insufficiency  there  is  an  associated  arterio- 
sclerosis and  the  systolic  blood-pressure  is  high. 

Pathological  Physiology. — Failure  of  the  aortic  valves  to  properly 
close  the  aortic  opening  results  in  the  back  flow  or  regurgitation  of  a 
portion  of  the  blood  which  has  been  thrown  into  the  systemic  arteries. 
The  problem  which  the  left  ventricle  faces  is  to  expel  during  each  systole 
the  normal  amount  of  blood  which  it  receives  from  the  left  auricle  plus 
the  amount  which  regurgitates  from  the  aorta.  This  naturally  increases 
its  work  and  results  in  hypertrophy.  The  latter  is  proportional  to 
the  amount  of  regurgitated  blood.  In  cases  which  are  recognizable 
clinically  the  hypertrophy  is  usually  of  an  extreme  grade.  Another 
change  produced  in  the  left  ventricle,  as  the  result  of  the  regurgitation 
from  the  aorta,  is  dilatation.  This  is  brought  about  by  the  increased 
amount  of  blood  it  is  forced  to  accommodate  during  diastole.  Just  as  in 
the  case  of  hypertrophy  the  degree  of  dilatation  is  dependent  on  the 
amount  of  the  regurgitant  flow  from  the  aorta.  In  spite  of  the  excessive 
amount  of  blood  the  left  ventricle  must  expel  at  each  systole,  it  empties 
itself  in  about  the  same  length  of  time  as  the  normal  ventricle,  although 
it  does  not  always  do  so  as  completely.  Whereas  in  aortic  stenosis  the 
left  ventricle  requires  an  increased  amount  of  time  to  empty  itself,  a 
shortening  of  the  systole  is  an  advantage  in  aortic  insufficiency,  as  it  then 
has  less  blood  to  handle  by  reason  of  the  curtailment  of  the  diastolic 
period. 

As  the  result  of  the  great  hypertrophy  of  the  left  ventricle  the  blood 
is  driven  into  the  aorta  with  tremendous  force.  This  produces  a  high 
systolic  pressure1  in  the  systemic  arteries.  On  (lie  other  hand,  the 
sudden  regurgitation  of  a  portion  of  the  blood  from  the  aorta  into  the  left 


678  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

ventricle  leads  to  a  sudden  recoil  of  the  blood  column  and  consequently 
to  a  low  diastolic  pressure.  The  filling  of  the  systemic  arteries  under 
great  pressure,  and  the  sudden  drop  in  this  pressure  due  to  the  regurgita- 
tion can  be  seen  in  the  short,  abrupt  pulsation  of  the  visible  arteries 
and  can  also  be  felt  by  palpating  the  radial  artery.  The  incessant  pound- 
ing of  the  hypertrophied  left  ventricle,  the  high  systolic  pressure  and  the 
low  diastolic  pressure  tend  to  produce  a  very  intermittent  blood  supply 
in  the  whole  arterial  system  and  especially  in  the  coronary  vessels.  The 
latter  result  is  particularly  serious  as  it  interferes  with  the  nutrition  of 
the  heart  muscle  and  this  eventually  leads  to  exhaustion  through  degen- 
erative changes.  When  the  left  ventricle  reaches  the  limit  of  hyper- 
trophy or  becomes  exhausted,  dilatation  ensues  and  with  it  relative 
insufficiency  of  the  mitral  valve.  This  in  turn  is  followed  by  the  usual 
phenomena  of  broken  compensation. 

Symptoms. — Aortic  regurgitation  may  exist  in  a  latent  form  for  years 
without  giving  rise  to  any  symptoms  whatsoever.  Among  the  earliest 
symptoms  noted  are  those  due  to  alternations  in  the  circulation,  espe- 
cially cerebral  anemia.  There  may  be  headaches,  attacks  of  vertigo  or 
flashes  of  light  before  the  eyes.  Anemia  is  often  a  marked  feature 
in  these  cases,  the  face  especially  presenting  a  pale  grayish  color.  Even 
prior  to  any  evidence  of  failing  compensation,  pain  may  be  a  prominent 
symptom.  It  may  be  in  the  nature  of  true  angina,  or  a  sense  of  sub- 
sternal oppression  and  pain,  or  it  may  be  an  annoying  palpitation  or 
throbbing  sensation  in  the  precordium.  Shortness  of  breath,  especially 
after  exertion,  is  often  the  first  symptom  noticed  by  the  patient.  Later, 
there  may  be  cough  and  occasionally  blood-streaked  sputum.  Cyanosis 
is  unusual  unless  there  is  an  associated  mitral  lesion. 

In  patients  subject  to  this  lesion,  distressing  dreams  and  sleep 
which  is  broken  at  frequent  intervals,  are  more  common  than  in  any  other 
form  of  heart  disease.  Mental  symptoms,  such  as  delirium,  halluci- 
nations and  even  suicidal  tendencies,  are  also  occasionally  encountered. 

In  cases  of  aortic  insufficiency,  sudden  death  is  not  infrequent  and 
may  occur  with  but  slight  premonitory  symptoms.  The  foregoing 
symptoms  are,  for  the  most  part,  somewhat  distinctive  of  aortic  valvular 
trouble.  Failure  to  maintain  compensation  may  be  brought  about  by 
a  gradual  weakening  of  the  left  ventricle  and  the  establishing  of  mitral 
incompetency.  The  symptoms  then  assume  the  character  of  those 
due  to  broken  compensation  from  any  cause,  although  the  symptoms 
peculiar  to  the  lesion  itself  may  become  accentuated. 

Physical  Signs. — Inspection. — A  diagnosis  of  aortic  insufficiency  can 
be  made  in  a  large  number  of  cases  from  inspection  alone.  This  is  due 
to  the  arterial  phenomena  which  constitute  the  most  distinctive  feature 
of  the  disease. 

All  of  the  peripheral  arteries  are  seen  to  strongly  pulsate.  Not 
only  is  this  true  of  the  large  superficial  vessels  but  even  the  small  arteries 
in  the  hand  and  face  may  be  seen  to  throb,  and  on  ophthalmoscopic 
examination  the  retinal  arteries  may  be  seen  pulsating.  The  arterial 
pulsation  may  be  so  strong  that  the  foot  is  jerked  when  the  knee  is  crossed 
or  the  head  may  be  moved  slightly  with  each  systole. 

In  addition  the  so-called  capillary  pulse  is  usually  present.  This  is 
caused  by  the  rapid  filling  and  emptying  of  the  capillaries. 

The  pulsatile  movement  may  even  reach  the  veins.     This  may  be 


ENDOCARDITIS  679 

noted  in  the  veins  in  the  back  of  the  hands.  The  phenomenon  may 
be  brought  out  by  holding  the  hand  so  as  to  drop  the  wrist.  This  aids 
in  filling  the  veins  and  if  pulsation  is  present  it  will  not  be  sharp  and  abrupt 
as  in  the  arteries,  but  slow  and  deliberate.  Capillary  pulsation  is  some- 
times seen  in  asthenic  conditions  accompanied  with  a  low  blood-pressure. 

In  well-marked  cases  the  apex  beat  is  displaced  downward  and  to 
the  left.  It  is  commonly  in  the  sixth  interspace  but  may  be  as  low 
as  the  seventh  in  the  anterior  axillary  line.  If  the  hypertrophy  is  well- 
marked,  the  cardiac  impulse  is  heaving  and  forcible  and  may  move  the 
entire  precordium.  In  children  and  young  adults  the  precordium  may 
bulge.     If  dilatation  has  occurred  the  impulse  is  diffuse  and  often  wavy. 

Palpation. — This  enables  one  to  appreciate  more  fully  the  forcible, 
heaving  character  of  the  impulse.  Thrills  are  not  constant  but  may  be 
felt  occasionally.  They  are  either  presystolic  or  systolic  at  the  apex  or 
diastolic  and  systolic  over  the  base  of  the  heart.  The  arteries  feel  large 
and  are  usually  thickened.  When  one  of  the  radial  arteries  is  palpated, 
the  pulse  beat  is  felt  to  impinge  against  the  finger  with  an  abrupt,  forcible 
stroke  and  immediately  recede,  hence  the  terms  water-hammer  or  collaps- 
ing pulse.  It  is  also  frequently  referred  to  as  the  Corrigan  pulse.  The 
features  of  this  type  of  pulse  are  sometimes  best  appreciated  by  grasping 
the  wrist  and  holding  it  up  above  the  level  of  the  heart,  thus  accentuating 
the  effect  of  gravity.  The  distention  of  the  large  vessels  at  the  root  of  the 
neck  may  be  so  marked  as  to  simulate  aneurism.  The  sphygmographic 
tracing  is  characteristic.  The  upstroke  is  high  and  almost  perpendicular 
and  forms  a  very  acute  angle  with  the  sharply  descending  downstroke 
(see  Fig.  131).  It  is  in  marked  contrast  to  the  sphygmographic  record 
of  aortic  stenosis  which  is  exactly  the  reverse,  namely  a  slow  and  low  up- 
stroke and  a  very  gradual  descent  of  the  downstroke.  Auricular  fibrilla- 
tion which  is  so  commonly  encountered  in  mitral  disease  is  not  common  in 
aortic  lesions  unless  dilatation  of  the  left  ventricle  and  auricle  supervenes. 

Percussion.- — The  area  of  cardiac  dulness  is  usually  increased  to  the  left 
and  in  extreme  cases  may  reach  the  anterior  axillary  line.  The  upper 
border  may  reach  the  third  rib.  There  is  usually  some  dulness  to  the  right 
of  the  sternum.  This  may  be  due  to  extreme  hypertrophy  of  the  left 
ventricle  which  causes  an  extension  of  the  whole  heart  to  the  right  or  it 
may  be  brought  about  by  dilatation  of  the  right  ventricle  when  compensa- 
tion is  no  longer  complete  (see  Fig.  172). 

In  some  cases  a  slight  area  of  dulness  may  be  made  out,  over  the  ster- 
nal end  of  the  second  right  intercostal  space  due  to  dynamic  dilatation  of 
the  aorta. 

Auscultation. — The  murmur  of  aortic  insufficiency  is  caused  by  the 
backward  rush  of  blood  from  the  aorta  into  the  left  ventricle  during  the 
ventricular  diastole.  While  the  seat  of  the  production  of  the  murmur  is 
over  a  point  close  to  the  left  border  of  the  sternum  opposite  the  third 
costal  cartilage  it  is,  as  a  rule,  not  best  heard  in  this  situation.  The 
punctual  maximum  for  the  murmur  of  aortic  incompetency  is  placed,  by 
most  authorities,  at  the  second  costal  cartilage  on  the  right,  although 
there  are  some  who  believe  that  the  murmur,  in  many  instances,  is  best 
heard  in  the  fourth  interspace  on  the  left  side  close  to  the  sternum.  Our 
experience  is  in  accordance  with  the  latter  view.  The  murmur  is  in  most 
instances  soft  and  low-pitched.  It  may  be  very  loud,  but  it  rarely  has  the 
coarse  rasping  quality  so  commonly  heard  in  other  valvular  murmurs 


680  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

although  at  times  it  has  a  distinct  musical  tone.  The  murmur  of  aortic 
insufficiency  is  transmitted  downward  along  the  right  border  of  the 
sternum  or  towards  the  cardiac  apex.  It  also  may  be  heard  upwards  along 
the  sternal  margin  as  far  as  the  sterno-clavicular  articulation  or  in  the 
carotids.  In  such  instances  there  is  usually  a  dilatation  of  the  aorta  asso- 
ciated with  stretching  of  the  aortic  ring.  In  well-marked  cases,  with  a 
loud  murmur,  it  may  be  heard  all  over  the  chest  (see  Figs.  194  and  196). 
In  some  cases  the  murmur  of  Duroziez  may  be  heard  over  one  of  the 
large  arteries,  such  as  the  femoral  This  murmur  is  said  never  to  occur 
except  in  the  presence  of  aortic  leakage.  Traube's  double  sound  is  some- 
times heard  in  cases  complicated  by  tricuspid  insufficiency. 

The  murmur  may  be  long  drawn  out  and  occupy  the  whole  of  diastole 
or  it  may  be  short  and  take  up  but  part  of  the  second  sound.  Generally 
speaking,  a  long  loud  diastolic  murmur  shows  a  considerable  degree  of 
pressure  kept  up  in  the  aorta,  which  is  desirable  and  a  proof  that  the  heart 
is  acting  with  vigor;  also  that  the  valve  leakage  is  not  excessive.  This  is 
a  favorable  augury.  A  weak  short  murmur  indicates  the  opposite  and 
may  be  a  note  of  impending  danger  although  there  are  many  exceptions 
to  this  (Broadbent). 

The  pulse  pressure  may  also  be  utilized  to  determine  the  degree  of 
damage.  In  order  to  maintain  the  mean  aortic  pressure  the  systolic 
pressure  must  be  abnormally  high  in  order  to  compensate  for  the  rapid 
fall  of  pressure  during  diastole.  The  pulse  pressure,  however,  serves  as  a 
useful  gauge  of  the  degree  of  the  leak  only  when  compensation  is  effective. 

In  some  instances  the  murmur  of  aortic  incompetency  is  heard  by  the 
unaided  ear  much  better  than  with  a  stethoscope  (Flint). 

Associated  with  the  diastolic  murmur  there  is  very  often  heard  a 
systolic  murmur.  This  is  usually  due  to  some  degree  of  obstruction  but 
it  not  infrequently  happens  that  a  systolic  murmur  may  occur  without 
stenosis.  This  is  explained  by  Rosenbach  as  follows :  At  the  beginning 
of  the  left  ventricular  systole  the  regurgitating  flow  has  not  entirely 
ceased  and  when  this  encounters  the  opposing  current  a  murmur,  systolic 
in  time,  is  produced. 

If  compensation  is  complete  the  first  sound  at  the  apex  is  usually 
clear.  If  dilatation  of  the  left  ventricle  occurs,  the  first  sound  at  the  apex 
is  replaced  by  a  systolic  murmur  due  to  relative  insufficiency.  If  com- 
pensation is  again  restored,  this  murmur  disappears  and  the  first  sound 
becomes  normal. 

In  a  very  considerable  percentage  of  cases  of  aortic  incompetency  there 
is  heard  at  the  apex  a  murmur  presystolic  in  time  and  which  is  usually 
referred  to  as  Flint's  murmur. 

Since  Flint's  time  several  hypotheses  have  been  advanced  to  explain 
the  mechanism  of  this  murmur.  (1)  That  the  regurgitant  stream  tends 
to  lift  the  great  anterior  mitral  curtain  and  so  to  obstruct  the  mitral  orifice 
at  the  end  of  diastole  as  to  impede  the  current  from  the  auricle.  (2) 
That  the  mitral  valve  is  thrown  into  vibration  by  the  two  currents,  the 
regurgitant  from  the  aorta  and  the  direct  from  the  auricle.  (3)  That  in 
the  absence  of  aortic  valve  disease,  but  in  the  presence  of  adherent  peri- 
cardium, vibrations  may  be  set  up  by  the  current  propelled  from  a  dilated 
and  hypertrophied  auricle  into  a  ventricle  whose  muscular  walls  are 
deficient  in  tone.  (4)  That  shortening  of  the  chordae  tendinese,  or 
dilatation  of  the  left  ventricle,  may  bring  about  a  vertical  narrowing  of 


ENDOCARDITIS  681 

the  aperture  through  which  the  blood  passes  from  auricle  to  ventricle,  the 
auricular  muscle  continuing  to  be  sufficiently  powerful  to  generate  a 
fluid  vein.1  The  differentiation  of  this  murmur  from  that  due  to  mitral 
stenosis  has  been  considered  under  the  latter  condition  (see  Fig.  136). 

Diagnosis. — If  due  consideration  is  given  to  the  arterial  phenomena  asso- 
ciated with  the  diastolic  murmur  heard  at  the  base  of  the  heart  little  or  no 
confusion  should  arise.  If,  however,  the  diagnosis  is  made  on  the  presence 
of  a  murmur  alone  mistakes  may  occur  as  a  diastolic  murmur  is  sometimes 
heard  in  other  conditions.  In  addition  to  aortic  regurgitation  a  diastolic 
murmur  may  be  heard  at  the  base  of  the  heart  as  the  result  of  insuffi- 
ciency of  the  pulmonary  valves.  This  murmur,  sometimes  called  the 
Graham  Steell  murmur,  is  associated  with  chronic  mitral  disease  and  is 
caused  by  stretching  of  the  conus  arteriosus  and  the  orifice  of  the  pul- 
monary artery.  The  time  and  location  of  the  murmur  are  all  that  it 
has  in  common  with  aortic  regurgitation.  In  Graves'  disease  a  diastolic 
bruit  is  sometimes  heard  over  the  sternum  and  rarely  a  cardio-respirator y 
murmur  is  diastolic  in  time.  The  chief  point  of  distinction  between  the 
murmur  of  aortic  insufficiency  and  other  occasional  murmurs  occurring 
during  the  diastolic  phase  is  the  presence  or  absence  of  the  arterial 
phenomena. 

It  is  not  easy  to  distinguish  between  aortic  regurgitation  due  to 
disease  of  the  semilunar  valves  and  relative  insufficiency  associated  with 
dilatation  of  the  aorta.  In  the  latter  condition  the  murmur  is  often 
transmitted  high  over  the  sternum  or  even  into  the  carotids;  in  addition 
there  is  dulness  to  the  right  in  the  second  interspace  due  to  the  dilated 
aorta. 

The  following  peripheral  arterio-venous  signs  may  be  met  with  in 
cases  of  aortic  insufficiency,  and  while  they  are  more  commonly  and  strik- 
ingly met  with  in  this  condition  than  in  any  other,  they  are  none  of  them 
pathognomonic  of  this  lesion.  (1)  Collapsing  pulse,  (2)  visible  arterial 
pulsation,  (3)  capillary  pulse,  (4)  venous  pulse,  (5)  hepatic  pulse,  (6) 
femoral  snap,  (7)  double  femoral  murmur  (Duroziez's  sign),  (8)  Double 
femoral  tones  (Traube's  sign).2 

AORTIC  STENOSIS 

Etiology. — This  is  the  rarest  of  the  left-sided  valvular  lesions.  True 
aortic  stenosis  unassociated  with  another  valvular  lesion  is  not  often 
encountered.  In  the  autopsy  records  of  the  Pennsylvania  and  Philadel- 
phia General  Hospitals,  Norris  found  48  instances  of  aortic  stenosis  out 
of  a  total  of  9940  cases  having  cardiac  lesions.  It  is  important  to  bear  this 
in  mind  as  a  systolic  murmur  at  the  aortic  cartilage  is  relatively  common 
and  on  this  evidence  alone  a  diagnosis  of  aortic  stenosis  is  made  far  too 
frequently.  The  interpretation  of  systolic  murmurs  heard  at  the  aortic 
area  has  been  considered  on  page  730.  The  great  majority  of  cases 
of  aortic  stenosis  are  encountered  in  those  past  the  middle  period  of  life 
and  in  those  who  are  the  subjects  of  atheromatous  changes  in  the  arteries, 
especially  the  aorta.  It  is  rare  among  women.  Occurring  as  a  single 
lesion  it  is  not  often  caused  by  acute  rheumatic  fever. 

1  Sansom  and  GlBSON,  Au.bittt  and  Rolleston:  "System  of  Medicine,"  vol.  vi, 
p.  362. 

2  Tick,  F. :  "The  Clinical  Determination  and  Significance  of  Some  Peripheral 
Signs  of  Aortic  Insufficiency,"  Illinois  Med.  Jour.,  September,  1911. 


682  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

Morbid  Anatomy. — The  anatomical  changes  which  take  place  in  the 
semilunar  valves  are  precisely  similar  to  those  which  occur  in  the  intima 
of  the  blood-vessels  and  ending  in  atheromatous  degeneration.  As  a 
result,  the  leaflets  become  fused,  stiff,  and  rigid  and  obstruct  the  free 
escape  of  the  blood  from  the  left  ventricle  into  the  aorta  (see  Fig. 
385).     In  some  instances  the  obstruction  is  made  worse  by  vegetations 


Fig.  385. — Aortic  obstruction  from  above.  The  margins  of  the  leaflets  are  fused  to- 
gether, thickened  and  calcified,  reducing  the  orifice  to  about  one-third  of  its  normal  caliber. 
The  mitral  and  tricuspid  orifices  are  also  sclerosed  and  contracted. 

which  develop  during  an  attack  of  secondary  endocarditis  (see  Fig. 
386).  The  resistance  offered  adds  to  the  work  of  the  left  ventricle  which, 
as  a  consequence,  becomes  hypertrophied.  It  is  in  this  variety  of  val- 
vular lesion  that  the  so-called  " concentric  hypertrophy"  is  most  nearly 
approximated.  Practically,  however,  some  degree  of  dilatation  is  always 
present.  When  the  heart  can  no  longer  overcome  the  obstruction,  dila- 
tation and  the  phenomena  of  broken  compensation  ensue. 


ENDOCARDITIS 


683 


Pathological  Physiology. — The  mechanism  of  aortic  stenosis  is  quite 
simple.  Owing  to  the  obstruction  to  the  ventricular  outflow,  the 
blood-pressure  in  the  left  ventricle  is  increased,  sometimes  to  twice 
the  normal.  Another  effect  caused  by  the  obstruction  is  to  prolong 
the  time  of  emptying  the  ventricle  and  as  a  result  the  ventricular  systole 
may  consume  from  5  to  50  per  cent,  more  than  the  normal  time.  If 
the  obstruction  become^  too  great  or  the  muscle  becomes  exhausted,  an 


FlG.   386. — Aortic  obstruction,  seen  from  above.      The  leaflets  are  fused  together,  thick- 
ened, and  indurated.     They  are  covered  with  small  vegetations. 


insufficient  amount  of  blood  reaches  the  systemic  circulation  and  as  a 
result  the  pulse  pressure  becomes  small  and  symptoms  of  cerebral 
anemia  may  develop.  In  cases  of  aortic  stenosis  the  left  ventricle 
occupies  the  same  position  in  maintaining  compensation  that  the  right 
ventricle  does  in  mitral  disease.  As  long  as  the  hypertrophy  keeps  in 
advance  of  the  obstruction,  the  circulatory  equilibrium  is  maintained. 
If,  however,  the  obstruction  becomes  too  great  or,  what  is  more  apt  to 


684  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

occur,  the  muscle  becomes  exhausted,  the  ventricle  dilates  and  then  there 
develops  relative  mitral  insufficiency  with  the  usual  sequence  of  events 
which  characterize  broken  compensation.  Some  observers  have  ex- 
pressed the  opinion  that  stretching  of  the  mitral  ring  and  a  certain 
amount  of  leakage  through  the  auriculo-ventricular  opening  is  to  be  looked 
upon  as  being  in  the  nature  of  a  safety  valve  action.  There  is  little  to  sup- 
port this  view,  however. 

Symptoms. — Of  all  the  valvular  lesions  aortic  stenosis  is  the  most  apt 
to  occur  in  a  latent  form.  It  may  be  present  for  years  without  causing 
serious  symptoms.  Failure  of  the  left  ventricle  manifests  itself  by  the 
occurrence  of  symptoms  which  may  be  brought  on  by  slight  exertion, 
or  excitement.  They  consist  of  shortness  of  breath,  palpitation,  a  sense 
of  oppression  in  the  precordium,  and  substernal  pain  or  anginal  attacks. 
In  addition  a  curtailment  of  the  amount  of  blood  thrown  into  the  sys- 
temic arteries  may  manifest  itself  by  evidences  of  cerebral  anemia,  such 
as  vertigo  or  dizziness.  If  the  left  ventricle  become  dilated  from  exhaus- 
tion, the  usual  phenomena  attending  broken  compensation  are  present. 
Sudden  death  is  not  uncommon  and  may  occur  as  the  result  of  sudden 
cardiac  failure  or  an  attack  of  angina. 

Physical  Signs. — Inspection  does  not  reveal  much  of  importance; 
extreme  hypertrophy  is  not  often  marked  as  a  result  of  this  lesion. 
Furthermore,  occurring  as  it  does  in  elderly  people,  the  size  of  the  heart 
is  often  obscured  by  a  rigid  chest  wall  and  emphysematous  lungs. 

Palpation. — A  very  common  feature  of  aortic  stenosis,  although  not 
peculiar  to  it,  is  a  systolic  thrill  felt  over  the  base  of  the  heart  on  the 
right  side.  One  of  the  most  distinctive  features  of  this  lesion  is  the  slow 
retarded  pulse  felt  at  the  wrist  and  graphically  shown  by  a  sphygmo- 
graphic  tracing.  The  pulse  is  often  slow,  between  50  and  60  beats  per 
minute  and  the  pulse  wave  is  much  prolonged.  This  is  well  shown  in  a 
pulse  tracing  but  may  also  be  appreciated  by  the  palpating  finger  as  the 
artery  is  gradually  filled  with  blood.  In  addition  to  the  slow  slanting  up- 
stroke the  tracing  may  show  an  anacrotic  pulse  or  the  pulsus  bisferiens. 

Percussion. — This  is  relatively  unimportant  and  is  often  valueless 
owing  to  pulmonary  emphysema. 

Auscultation. — As  we  have  repeatedly  emphasized,  a  systolic  murmur 
at  the  aortic  area,  even  when  transmitted  to  the  vessels  in  the  neck,  is 
not  pathognomonic  of  true  stenosis  but  is  more  often  associated  with 
changes  in  the  aorta  itself,  usually  a  roughening  of  the  intima  or  a  dilata- 
tion of  the  artery.  The  murmur  of  true  aortic  stenosis  is  transmitted 
not  only  upward  to  the  carotids  but  is  frequently  audible  along  the  right 
border  of  the  sternum  as  low  as  the  fourth  or  fifth  ribs.  In  some  in- 
stances it  is  very  loud  and  may  be  heard  all  over  the  precordium  and  in 
such  instances  the  question  always  arises  as  to  whether  the  murmur 
heard  at  the  apex  is  the  same  as  that  heard  at  the  aortic  cartilage  or 
is  a  second  murmur  due  to  mitral  insufficiency.  Even  more  distinctive 
of  stenosis  than  the  slow  retarded  pulse  is  the  character  of  the  second 
aortic  sound.  This  is  either  very  feeble  or  inaudible  due  to  the  fact  that 
the  stiff  and  rigid  valve  segments  are  incapable  of  snapping  together. 
If,  therefore,  the  second  aortic  sound  is  normal  and  especially  if  it  is 
loud  and  ringing  in  character,  the  murmur  originates  in  the  aorta  and  is 
not  due  to  rigid  and  diseased  valves.  Some  leakage  is  probably  always 
present  but  this  is  often  so  slight  that  no  murmur  can  be  heard. 


ENDOCARDITIS  685 

Diagnosis. — The  diagnosis  of  true  aortic  stenosis  rests  upon  the  fol- 
lowing facts:  (1)  A  systolic  thrill  felt  over  the  base  of  the  heart  to  the 
right  of  the  sternum;  (2)  a  slow  retarded  pulse;  (3)  a  systolic  murmur 
heard  at  the  aortic  cartilage  and  transmitted  to  the  vessels  of  the  neck; 
and  last,  but  most  important,  a  feeble  or  inaudible  second  aortic  sound. 

TRICUSPID  INSUFFICIENCY 

Etiology. — Lesions  involving  the  tricuspid  valve  may  be  (1)  organic 
and  (2)  functional. 

1.  Organic  disease  of  the  tricuspid  leaflets  is  rare  although  not  so  un- 
usual as  was  once  believed  to  be  the  case.  Formerly  it  was  taught  that 
organic  lesions  of  the  valves  in  the  right  heart  were  almost  invariably 
congenital  in  origin.  Recent  investigations,  however,  have  shown  that 
these  lesions  are  more  frequently  the  result  of  acquired  disease  than  of  a 
congenital  defect. 

(a)  The  tricuspid  leaflets  may  be  the  seat  of  an  acute  inflammatory 
process  which  develops  during  the  course  of  one  of  the  acute  infections 
such  as  puerperal  fever  and  other  forms  of  general  sepsis,  gonorrhea, 
pneumonia,  diphtheria,  scarlet  fever  and  acute  rheumatic  fever.  The 
last-named  infection  is  by  far  the  most  important  etiological  factor. 
Statistical  studies  indicate  that  acute  rheumatic  fever  is  the  apparent 
cause  of  organic  tricuspid  disease  in  from  35  to  62  per  cent,  of  cases.1 
Occasionally  the  acute  endocarditis  is  limited  to  the  tricuspid  leaflets 
but  in  the  majority  of  cases  it  is  associated  with  similar  lesions  of  the 
aortic  or  mitral  valves,  especially  the  latter;  with  few  exceptions  the 
valves  in  the  left  heart  are  the  sites  of  old  lesions. 

(b)  Thickening  of  the  tricuspid  leaflets  as  the  result  of  fibrosis  occurs 
under  practicalljr  the  same  circumstances  as  similar  lesions  affecting  the 
mitral  valve. 

(c)  The  organic  lesion  may  be  the  result  of  rupture  of  one  of  the  leaf- 
lets or  chordae  tendinese  following  a  blow  on  the  chest  or  unusual  muscu- 
lar effort.     This  is  extremely  rare. 

2.  Functional  or  Relative  Tricuspid  Insufficiency. — This  is  extremely 
common  and  may  arise  in  a  large  number  of  conditions.  The  functional 
efficiency  of  the  tricuspid  valve  depends  very  largely  upon  the  tone  of 
the  sphincter-like  muscular  fibers  surrounding  the  orifice.  It  has  long 
been  recognized  that  from  a  mechanical  standpoint  the  tricuspid  valve 
is  much  inferior  to  the  mitral.  Even  a  slight  degree  of  dilatation  of  the 
right  ventricle  induces  incompetency.  This  is  due  not  only  to  relaxation 
of  the  tricuspid  sphincter,  but  more  especially  to  the  fact  that  in  dilated 
hearts  the  origin  of  the  chordae  tendinese  and  the  papillary  muscles  are 
too  far  from  the  center  of  the  ventricular  cavity  to  permit  perfect  valvu- 
lar closure  (Krehlj.  Indeed  Mackenzie  inclines  to  the  opinion  that  the 
tricuspid  valve  is  barely  able  to  close  the  orifice  perfectly  and  that  the 
slightest  disturbance  will  cause  some  leakage.  Thus  the  transient  tachy- 
cardia which  sometimes  results  from  the  excitement  incident  to  a  physical 
examination  may  be  accompanied  by  a  tricuspid  systolic  murmur  which 
is  usually  very  fugitive  and  disappears  when  the  heart  becomes  quieter. 

1  Griffith:  Edinburgh  Med.  Jour.,  1903,  lv,  105.  Herrick:  Boston  Med.  and 
Surg.  Jour.,  1897,  cxxxvi,  245.  Leudet:  Paris  Thesis,  1881.  Norms:  ''Studies  in 
Cardiac  Pathology,"  1911.      Pitt:   "Allbutt's  System  of  Medicine,''  2d  ed. 


686  DISEASES    OF   THE    PERICARDIUM,    HEART,    AND    AORTA 

The  ease  with  which  regurgitation  occurs  through  the  right  auriculo- 
ventricular  orifice  is  considered  by  some  to  be  in  the  nature  of  a  safety 
valve,  whereby  the  thin  wall  of  the  right  ventricle  is  relieved  of  undue 
tension.  Experimentally  it  is  not  possible  to  raise  the  tension  in  the 
right  ventricle  on  account  of  the  ease  with  which  leakage  occurs  through 
the  tricuspid  orifice  (see  Figs.  205  and  206). 

The  essential  factor  in  the  production  of  functional  tricuspid  insuffi- 
ciency, therefore,  is  an  increase  in  tension  which  in  turn  tends  to  dilate 
the  right  heart.  This  may  be  brought  about  by  work  which  necessitates 
great  muscular  and  intrathoracic  straining,  asphyxia,  obstruction  in  the 
pulmonary  circulation,  such  as  may  occur  in  chronic  inflammatory  affec- 
tions of  the  lungs  and,  lastly,  and  most  important,  by  disease  of  the  heart 
itself.  Dilatation  of  the  right  ventricle  and  functional  tricuspid  insuffi- 
ciency inevitably  occur  whenever  failing  compensation  arises  as  the  result 
of  chronic  valvular  or  myocardial  disease.  Disease  of  the  mitral  valve 
is  especially  apt  to  bring  about  these  conditions.  Slight  degrees  of  tri- 
cuspid insufficiency  are  also  of  frequent  occurrence  in  all  diseases  in  which 
the  nutrition  of  the  cardiac  muscle  suffers.  Among  such  diseases  may 
be  mentioned  the  acute  specific  fevers,  diabetes,  the  cachexia  accom- 
panying malignant  disease,  and  severe  anemia.  It  is  probable  that 
some  degree  of  tricuspid  insufficiency  occurs  in  every  dying  or  failing 
heart. 

Morbid  Anatomy. — When  the  insufficiency  is  due  to  organic  disease 
of  the  valves,  the  lesions  are  essentially  the  same  as  occur  in  the  mitral 
valve.  The  leaflets  may  be  deformed  or  may  be  the  seat  of  fibroid  changes, 
vegetations  or  ulcerations.  The  changes  occur  oftenest  on  the  free  mar- 
gin of  the  middle  portion,  with  the  anterior  portion  next  in  frequency. 
The  chordse  tendinese  are  often  attenuated  and  elongated  and  the  tip  of 
the  papillary  muscle  not  infrequently  is  indurated.  The  tricuspid  opening 
is  enlarged. 

Whether  the  incompetency  is  due  to  organic  disease  or  functional 
incapacity  of  long  standing  the  right  auricle  is  much  dilated  and  globular 
in  appearance  and  the  right  ventricle  is  also  much  dilated.  The  ventricle 
may  show  also  a  certain  amount  of  muscular  hypertrophy.  Inasmuch 
as  the  lesion  produces  a  damming  back  of  blood  in  the  venous  system  the 
viscera  (liver,  spleen  and  kidneys)  show  evidences  of  chronic  congestion. 
If  the  congestion  of  the  liver  is  constant,  degeneration  and  atrophy  of  the 
liver  cells  as  the  result  of  pressure  often  occurs,  producing  a  condition 
known  as  the  " nutmeg"  liver. 

Pathological  Physiology. — The  first  effect  of  tricuspid  regurgitation  is 
to  distend  the  right  auricle.  As  the  wall  of  this  chamber  is  very  thin  and 
contains  but  little  muscular  structure,  dilatation  quickly  ensues  if  the 
back  flow  is  prolonged.  As  the  right  auricle  is  unable  to  withstand  the 
pressure  the  blood  is  dammed  back  into  the  venae  cavse  giving  rise  to  the 
characteristic  features  of  tricuspid  insufficiency.  The  venous  stasis 
which  results  may  give  rise  of  edema  of  the  extremities  and  effusions  into 
the  serous  cavities  (see  "  Hydrothorax, "  p.  564  also  Figs.  109,  206);  to 
congestion  of  the  kidneys  causing  diminished  excretion  of  urine  which 
contains  large  quantities  of  albumen  and  casts ;  to  congestion  of  the  liver 
which  becomes  enlarged,  painful  and  often  pulsatile;  and  to  congestion 
of  the  face  and  pulsation  of  the  jugulars.  In  addition  an  asphyxial  condi- 
tion may  be  produced  by  stasis  in  the  medulla  oblongata. 


ENDOCAEDITIS  687 

Stadler1  has  shown  experimentally  in  rabbits  that  tricuspid  insuffi- 
ciency, if  marked,  leads  to  dilatation  and  hypertrophy  of  both  the  right 
auricle  and  ventricle  and  to  atrophy  of  the  left  ventricle,  due  apparently 
to  the  smaller  amount  of  blood  handled.  In  the  less  severe  lesions  the 
tricuspid  insufficiency  is  apparently  compensated  for  by  increased  vascu- 
lar tone  and  hypertrophy  of  the  right  auricle,  which  not  only  contracts 
more  forcibly  but  aspirates  blood  from  the  veins  more  powerfully. 

Symptoms. — When  the  tricuspid  insufficiency  is  transient,  such  as 
occurs  as  the  result  of  slight  excitement,  there  are  no  symptoms.  In  well- 
defined  cases  the  most  constant  symptom  is  dyspnea.  This  may  become 
manifest  only  after  exertion  but  in  extreme  cases  it  is  apparent  even  when 
the  patient  is  at  rest.  In  severe  cases  the  patient  may  be  orthopneic  and 
often  is  drowsy.  The  slightest  exertion  causes  fatigue.  Precordial  pain 
is  not  often  complained  of  but  there  may  be  a  sense  of  oppression  in  the 
chest.  Pain  over  the  liver  is  a  common  and  important  symptom.  It  is 
caused  by  engorgement  of  the  liver  and  stretching  of  the  capsule.  If  the 
engorgement  is  of  long  standing,  the  patient  may  be  slightly  jaundiced. 
Associated  with  the  hepatic  pain  there  is  often  anorexia,  nausea  and  vomit- 
ing and  eructations.  It  not  infrequently  happens  that  the  prominence 
of  the  gastric  symptoms  deceives  a  careless  observer  into  the  belief  that 
the  stomach  is  the  real  seat  of  the  patient's  symptoms. 

Edema  of  the  lower  extremities  is  common.  The  condition  is  less 
evident  after  a  night's  rest  in  bed.  Ascites  and  effusions  into  the  serous 
cavities  of  the  thorax  may  occur  alone  or  in  association  with  the  edema. 
The  urine  is  scanty  and  contains  both  albumen  and  casts.  The  chest 
should  always  be  carefully  examined  in  patients  suffering  from  tricuspid 
regurgitation  as  effusions  into  the  pleural  sacs,  especially  the  right,  are 
common  and  may  be  responsible  for  much  of  the  dyspnea. 

Physical  Signs. — Inspection. — In  a  patient  with  well-marked  tricuspid 
insufficiency  cyanosis  is  a  marked  feature.  The  face  has  a  livid  hue  while 
the  lips,  tips  of  the  ears  and  finger  ends  are  bluish  in  color.  If  the  ven- 
ous stasis  is  of  long  standing  the  conjunctiva  may  have  an  icteroid  tinge 
or  the  skin  may  be  slightly  jaundiced.  .  The  latter  symptom  is  always  of 
ominous  import.  The  veins  of  the  neck,  arms  and  chest  are  often  dilated. 
In  some  cases  a  distinct  systolic  pulsation  of  the  liver  is  visible.  Edema 
of  the  extremities  and  genitalia  is  commonly  present  (see  Figs.  208,  380). 

The  cardiac  impulse  is  often  diffuse  and  the  apex  beat  is  seen  or  felt 
beyond  the  mid-clavicular  line.  Marked  cardiac  pulsation  due  to  the 
hypertrophied  right  ventricle  may  be  seen  on  the  right  side  between  the 
sternal  and  parasternal  line. 

Pulsation  in  the  jugular  veins  is  an  important  diagnostic  sign.  Even 
without  tracings  three  pulsations  may  be  seen  in  the  supraclavicular 
triangle.  (1)  A  wave  appearing  slightly  before  the  impulse  at  the  apex 
beat,  due  to  pulsation  of  the  right  auricle;  (2)  a  wave  which  is  synchron- 
ous with  the  beat  in  the  carotid  artery,  as  felt  higher  up  in  the  neck;  (3) 
a  wave  occurring  immediately  after  systole  of  the  ventricle,  the  ventricu- 
lar wave  (Osier  and  Gibson).  The  ventricular  wave  is  produced  as  fol- 
lows: When  the  tricuspid  insufficiency  has  become  marked  the  regurgita- 
tion of  blood  becomes  too  great  for  the  auricle  to  contain.  The  latter 
dilates  to  such  an  extent  that  the  orifices  of  the  veins  emptying  into  it 
cannot  be  closed.  As  a  result  there  is  during  each  systole  of  the  right 
1  Deut.  Arch.  f.  Klein.  Med.,  1905,  lxxxiii,  1  and  2. 


DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

ventricle  an  unobstructed  path  from  the  ventricle  to  the  veins.  Such 
being  the  case,  with  each  contraction  of  the  right  ventricle  the  impulse  of 
the  blood  regurgitating  through  the  tricuspid  opening  is  imparted  to  the 
blood  in  the  jugulars.  In  like  manner  the  systolic  pulsation  of  the  liver 
is  also  produced.  When  the  leakage  becomes  very  marked,  the  auricle 
becomes  paralyzed  and  the  auricular  fibrillation  is  present.  The  transi- 
tion of  the  normal  venous  pulse  to  that  characterized  by  the  ventricular 
pulse  is  shown  diagrammatically  in  Fig.  387. 


Fig.  387. — Diagram  to  show  the  transition  from  the  normal  venous  pulse  to  the  ventric- 
ular form,  i.  e.,  in  tricuspid  insufficiency.  I  is  the  normal  venous  pulse  from  which  the  c 
wave,  occurring  between  a  and  v,  probably  due  to  the  carotid  artery,  has  been  omitted; 
a  auricular  wave;  v.  ventricular  wave,  whose  significance  in  the  normal  venous  pulse  is 
doubtful.     E,  period  of  outflow  into  the  pulmonary  artery.     (After  Mackenzie.) 

Palpation. — Marked  pulsation  may  be  felt  over  the  epigastrium  and 
to  the  right  of  the  sternum  in  the  fourth  and  fifth  interspaces.  A  systolic 
thrill  is  often  felt  and  occasionally  a  slight  systolic  shock  may  be  per- 
ceived. Pulsation  may  be  felt  over  the  liver.  When  the  liver  is  enlarged 
the  surface  is  smooth  and  the  edge  firm  and  sharp.  The  radial  pulse 
is  usually  small,  weak  and  often  irregular.  The  blood-pressure  is  normal 
or  slightly  below  normal. 

Percussion. — The  area  of  cardiac  dulness  is  increased  in  the  transverse 
diameter,  especially  to  the  right  of  the  sternum.  In  extreme  cases  the 
dulness  may  extend  three  fingers'  breadth  or  more,  to  the  right  of  the 
sternum.  Relative  tricuspid  insufficiency  is  believed  by  some  to  produce 
a  wider  area  of  dulness  than  is  the  case  if  an  organic  lesion  is  present. 

Auscultation.- — The  punctum  maximum  of  a  tricuspid  murmur  due  to 
insufficiency  is  over  the  middle  of  the  lower  part  of  the  sternum.  It  is 
systolic  in  time  and  may  be  best  heard  a  little  to  the  left  or  a  little  to  the 
right  of  the  sternum;  and  if  hypertrophy  of  the  right  ventricle  is  marked; 


ENDOCARDITIS  689 

it  may  be  audible  all  over  the  precordium.  In  those  cases  of  relative  in- 
sufficiency of  brief  duration  the  murmur  is  the  only  evidence  of  tricuspid 
leakage  we  possess.  On  the  other  hand,  it  is  to  be  borne  in  mind  that  an 
extreme  degree  of  regurgitation  may  be  present  without  a  murmur  being- 
heard.  A  weak  muscle  and  a  widely  dilated  orifice  may  not  produce  a 
bruit. 

If  due  to  organic  disease,  the  murmur  may  be  rough  in  character. 
When  due  to  relative  insufficiency,  the  murmur  is  usually  soft  and  blowing 
in  character.  The  tricuspid  murmur  is  not  often  transmitted  far  from  the 
area  of  maximum  intensity.  Occasionally  it  is  heard  as  far  as  the  pul- 
monary area.  It  may  be  transmitted  to  the  right  and  at  times  is  audible 
posteriorly  near  the  angle  of  the  right  scapula.  The  murmur  may  replace 
all  or  part  of  the  first  sound.  The  character  of  the  sounds  at  the  base 
of  heart  vary  considerably.     They  may  be  feeble  or  accentuated. 

Diagnosis. — The  diagnosis  of  tricuspid  insufficiency  depends  on  the 
presence  of  increased  cardiac  dulness  to  the  right  of  the  sternum;  a 
systolic  murmur  best  heard  at  the  xiphoid  cartilage;  a  venous  pulse  of  the 
ventricular  type;  pulmonary  congestion  and  enlargement  of  the  liver  with 
systolic  pulsation. 

If  the  regurgitation  is  functional  in  type  and  due  to  trivial  causes  there 
may  be  nothing  to  indicate  the  condition  except  a  soft,  blowing  murmur, 
transient  in  character.  If,  on  the  other  hand,  the  functional  derangement 
is  severe,  there  may  be  no  murmur  as  the  widely  dilated  orifice  and  weak 
muscle  do  not  permit  of  sufficient  driving  force  to  cause  a  murmur.  In 
such  cases  the  diagnosis  depends  on  the  presence  of  the  ventricular  type 
of  pulse,  enlarged  right  heart  and  engorged  liver.  If  the  murmur  is  organic 
in  origin,  it  will  be  rough  in  character  and  as  compensation  is  restored  will 
persist  instead  of  disappearing  as  is  the  case  with  murmurs  due  to  relative 
insufficiency. 

If  the  tricuspid  murmur  exists  alone,  which  is  rarely  the  case,  there  is 
little  difficulty  in  determining  its  origin.  As  a  rule,  however,  it  is  com- 
bined with  other  murmurs  and  in  such  cases  the  punctum  maximum  of 
each  murmur  must  be  determined. 


TRICUSPID  STENOSIS 

Etiology. — Stenosis  of  the  tricuspid  orifice  is  relatively  rare  and  for 
the  most  part  is  first  recognized  at  the  autopsy  table.  The  lesion  rarely 
exists  alone.  W.  W.  Herrick1  has  collected  187  cases  and  of  this  number 
the  tricuspid  valve  was  involved  alone  in  14.  In  102  there  was  disease 
of  the  mitral  valve  as  well  and  in  64  the  aortic  valve  was  also  involved. 
At  the  Philadelphia  General  Hospital  among  8640  autopsies  Norris  found 
8  cases  of  tricuspid  stenosis  recorded. 

The  most  important  etiological  factors  are  acute  rheumatic  fever  and 
chorea.  In  Herrick's  series  61  cases  gave  a  definite  history  of  acute 
rheumatic  fever  and  in  11  more  there  was  a  doubtful  history  of  this  in- 
fection or  chorea.  Pitt  found  the  incidence  of  acute  rheumatic  fever  to 
be  as  high  as  62.06  per  cent.  Syphilis  has  been  believed  to  be  the  exciting- 
cause  in  a  few  cases.  Rarely  a  tumor  or  a  fibrinous  ball  may  obstruct 
the  tricuspid  orifice. 

1  Arch.  Int.  Med.,  1908,  ii,  295. 


690  DISEASES    OF   THE    PERICARDIUM,    HEART,    AND    AORTA 

Hirschf elder1  believes  that  when  the  tricuspid  stenosis  is  associated 
with  mitral  stenosis  the  same  etiological  factors  are  concerned.  "In 
view  of  the  work  of  Goodhart,  Roy  and  Aclami,  and  Weber  and  Degny, 
it  is  not  unlikely  that  the  overstrain  of  the  right  ventricle,  brought  about 
by  the  latter  conditions,  leads  to  edema  and  hemorrhage  into  the  tricus- 
pid valve,  and  that  these  processes  usher  in  fibrosis.  In  other  words, 
the  mitral  stenosis  itself  becomes  an  etiological  factor  in  the  tricuspid 
lesion,  and  the  pathological  process  completed  in  the  mitral  is  now  trans- 
ferred back  one  step  in  the  circulation  and  repeats  itself  in  the  tricuspid." 

Pitt2  gives  the  following  age  distribution  in  109  cases: 

Under  10  years ,    1  case 

Between  11  and  20  years 19  cases 

Between  21  and  30  years 41  cases 

Between  31  and  40  years  :.<•;.'.'... 29  cases 

Between  41  and  50  years 12  cases  - 

Between  51  and  60  years 4  cases 

Between  61  and  70  years. 3  cases 

109  cases 

As  but  one  of  the  109  cases  was  under  ten  years  of  age,  the  belief  once 
currently  held  that  such  lesions  are  commonly  congenital,  does  not  receive 
much  support. 

Tricuspid  stenosis  is  much,  more  frequent  in  women  than  men.  In 
Herrick's  series  there  were  133  women  and  38  men. 

Morbid  Anatomy.— As  to  the  valves  themselves  the  structural  changes 
are  analogous  to  those  found  in  the  mitral  valve  when  stenosis  is  present. 
There  may  be  vegetations  or  sclerosis,  and  changes  in  the  chordae  tendi- 
nese  or  papillary  muscles.  Obstruction  of  the  tricuspid  orifice  is  similar 
to  that  occurring  in  the  mitral  except  that  such  high  degrees  of  contrac- 
tion are  rarely  found;  nearly  always  the  opening  will  admit  two  fingers 
(see.Figs^  388  and  389). 

The  condition  of  the  heart  will  depend  on  the  duration  of  the  obstruc- 
tion. During  the  first  stage  there  will  be  some  hypertroplry  of  the  auricu- 
lar wall  and  of  the  superior  vena  cava.  At  a  later  stage  the  caval  open- 
ing is  found  to  be  greatly  enlarged,  so  that  the  auricle  and  the  veins  form 
a  continuous  sac.  The  auricular  wall  then  atrophies  and  may  become 
a  mere  fibrous  sac  formed  by  the  endocardium  and  epicardium.  Peri- 
carditis, sometimes  acute,  but  more  frequently  of  the  chronic  adhesive 
type,  is  a  very  common  finding. 

Owing  to  the  fact  that  mitral  stenosis  is  almost  constantly  associated 
with  tricuspid  stenosis  (85  out  of  87  cases  analyzed  by  Pitt)  it  is  often 
difficult  to  determine  how  much  or  how  little  effect  the  mitral  lesion  has 
had  in  bringing  about  the  secondary  changes  in  the  heart. 

The  liver  usually  presents  the  appearance  of  chronic  stasis  but  is  not 
always  enlarged.  The  liver  may  in  fact  be  smaller  than  normal  as  the 
result  of  cirrhosis  and  perihepatitis  due  to  the  prolonged  stasis. 

Pathological  Physiology. — With  the  onset  of  the  stenosis  the  wall  of 
the  right  auricle  hypertrophies  as  the  result  of  the  increased  amount  of 
work  it  has  to  perform.  Owing  to  the  increased  strength  of  the  right 
auricle  the  auricular  or  presystolic  wave  is  large  and  well  marked.     Mac- 

1  "Diseases  of  the  Heart  and  Aorta,"  2d  ed. 

2  Allbtjtt  and  Rolleston:  "System  of  Medicine,"  vol.  vi,  p.  331. 


ENDOCARDITIS  691 

kenzie  refers  to  a  case  in  which  the  auricle  had  become  so  greatly  hyper- 
trophied  that  it  sent  back  a  large  wave  into  the  jugular  vein,  and  with 
such  force  that  he  was  able  to  hear  the  valves  in  the  jugular  and  sub- 
clavian veins  close  with  a  snap.  Hypertrophy  of  the  right  auricle  also 
sends  a  wave  back  into  the  veins  with  such  force  that  distention  of  the 


Fig.  388.  Stenosis  of  the  aortic,  mitral,  and  tricuspid  valves.  The  aortic  leaflets 
are  fused  together  and  the  orifice  is  greatly  reduced  in  caliber.  The  mitral  orifice  consists 
of  a  mere  slit,  of  crescentic  outline — buttonhole  type.  The  tricuspid  orfice  is  also  con- 
tracted.     {Specimen  from  the  Philadelphia  Hospital.) 

liver  and  pulsation  of  that  organ  is  brought  about.  Later  when  the 
auricle  becomes  overdistended  and  paralyzed,  the  veins  remain  per- 
manently full  and  cease  to  pulsate.  Damming  back  of  the  blood  in  the 
veins  increases  the  pressure  in  these  vessels;  interferes  with  the  circula- 
tion of  the  blood  through  the  heart  and  lungs;  produces  cyanosis;  and 
finally  may  cause  polycythemia. 


692 


DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


The  slightest  overstrain  may  aggravate  the  venous  stasis  and  bring 
about  extreme  dyspnea,  cyanosis,  edema  and  effusions  into  the  serous 
cavities.  These  symptoms  may  pass  off  quickly  when  the  patient  is 
put  at  rest. 


Fig.  389. — Acute  and  chronic  endocarditis  of  the  aortic,  mitral,  and  tricuspid  valves. 
The  upper  portion  of  the  auricles  has  been  cut  away.  The  three  valvular  orifices  thus 
exposed  show  induration  and  contraction  of  their  component  tissues.  The  mitral  valve 
in  addition  shows  a  large  dark  mass  of  vegetations  of  recent  origin  which  almost  com- 
pletely occlude  its  orifice.  The  endocardium  and  myocardium  of  both  auricles  are  thick- 
ened.     {Photograph  by  Dr.  Alfred  R.  Allen.) 


ENDOCARDITIS  693 

Symptoms. — Pitt  gives  the  symptoms  of  tricuspid  stenosis  in  the 
order  of  their  relative  frequency  as  follows:  dyspnea,  edema,  albuminu- 
ria, enlarged  and  tender  liver,  and  cyanosis.  Dyspnea  is  almost  in- 
variably present;  edema  and  albuminuria  in  two-thirds  of  the  cases;  and 
enlarged  liver  and  extreme  cyanosis  in  one-half  of  the  cases.  Pain  radi- 
ating down  the  arms  or  over  the  hepatic  region  is  quite  common.  Hem- 
optysis is  not  infrequent  but  is  to  be  looked  upon  as  being  due  to  the 
associated  mitral  lesion. 

The  lesion  may  exist  for  years  without  causing  symptoms  or  at  the 
most,  slight  shortness  of  breath  on  exertion. 

Physical  Signs. — Inspection. — More  or  less  cyanosis  is  present;  in 
some  cases  it  is  very  marked.  In  addition  to  the  cyanosis  the  patient 
often  has  a  congested  appearance  due  to  polycythemia.  The  red  count 
may  be  as  high  as  8,000,000  or  9,000,000  per  cubic  millimeter.  Clubbing 
of  the  fingers  is  often  a  marked  feature.  The  veins  in  the  lower  part  of 
the  neck  are  usually  dilated  and  the  jugular  bulb  may  stand  out  promi- 
nently. It  will  be  recalled  that  the  venous  pulse  in  tricuspid  regurgita- 
tion is  ventricular  in  origin  and  systolic  in  time;  that  in  tricuspid  steno- 
sis is  auricular  in  origin  and  presystolic  in  time.  Mackenzie  considers 
pulsation  of  the  liver  with  a  marked  wave  due  to  the  auricle  as  an  evi- 
dence of  possible  tricuspid  stenosis.  When  the  auricle  becomes  overdis- 
tended  and  paralyzed  the  pulsation  disappears. 

As  tricuspid  stenosis  is  almost  invariably  associated  with  stenosis  of 
the  mitral  valve,  it  is  difficult  to.  determine  which  lesion  is  most  respon- 
sible for  the  diffuse  area  of  pulsation  and  displacement  of  the  apex  beat 
to  the  left.  .   . 

Palpation. — In  some  instances  a  thrill,  presystolic  or  systolic  is  felt 
over  the  lower  part  of  the  sternum. 

Percussion. — The  transverse  diameter  of  cardiac  clulness  is  always 
increased,  especially  to  the  right  of  the  sternum. 

Auscultation. — It  is  only  rarely  that  a  presystolic  tricuspid  murmur 
is  heard  and  for  this  reason  the  diagnosis  is  not  often  made  during  life. 
In  Leudet's1  series  of  114  cases  the  diagnosis  was  made  before  death  in 
but  6  instances.  The  murmur  when  present  is  best  heard  at  or  to  the 
left  of  the  xiphoid  cartilage;  is  presystolic  in  time;  and  is  not  transmitted. 
Although  rough  in  character,  it  is  less  harsh  than  the  mitral  presystolic 
murmur.  Pitt  states  that  a  presystolic  murmur  has  been  noted  in  less 
than  10  per  cent,  of  the  cases  and  that  a  localized  systolic  murmur  has 
been  much  more  frequently  noted.  In  half  the  cases  there  is  no  murmur 
at  the  tricuspid  area. 

Diagnosis. — This  cannot  be  made  with  any  certainty.  The  condition 
is  to  be  suspected  if  there  be  marked  cyanosis,  clubbing  of  the  fingers, 
dyspnea,  edema  of  the  extremities,  auricular  pulsation  of  the  jugulars 
and  liver  and  the  presence  of  a  presystolic  murmur  over  the  lower  part 
of  the  sternum. 

PULMONARY  INSUFFICIENCY 

Etiology. — This  is  a  rare  lesion.  Norris  found  but  one  case  among 
8640  autopsies  at  the  Philadelphia  General  Hospital  and  Hirschfelder 
records  3  cases  among  24,000  medical  admissions  to  the  Johns  Hopkins 

1  Paris  Thesis,  1881. 


694  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

Hospital.  Pitt,  in  1910,  placed  the  total  number  of  eases  on  record 
as  109. 

The  lesion  affects  both  sexes  equally,  may  occur  at  any  age,  but  in 
the  great  majority  of  cases  it  occurs  in  adult  life. 

Pulmonary  insufficiency  may  occur:  (1)  As  the  result  of  an  acute 
endocarditis.  The  infecting  organism  is  usually  the  streptococcus, 
pneumococcus  or  the  gonococcus.  Pitt  has  called  attention  to  the  relative 
frequency  of  gonorrheal  endocarditis  affecting  the  pulmonary  valve. 
(2)  In  association  with  aneurism  of  the  aorta  in  which  the  inflammatory 
change  in  the  neighborhood  of  the  pulmonary  artery  causes  an  adhesion 
of  one  or  more  cusps  of  the  pulmonary  valve  to  it  (Pitt).  (3)  As  the 
result  of  fibroid  changes  in  the  valve  leaflets.  The  fibrosis  may  produce 
insufficiency  alone  or  it  may  be  associated  with  stenosis.  (4)  As  the 
result  of  congenital  malformation  or  rupture  of  a  leaflet.  (5)  Relative 
insufficiency  may  occur  if  pressure  in  the  pulmonary  artery  is  much  in- 
creased. This  may  arise  in  association  with  any  condition  which  pro- 
duces long-continued  pulmonary  hypertension,  such  as  emphysema, 
chronic  pulmonary  disease  and  especially  mitral  stenosis.  Graham 
Steell  has  emphasized  the  frequency  with  which  dilatation  occurs  in 
association  with  mitral  stenosis. 

Pathological  Physiology. — Incompetence  of  the  pulmonary  valve 
leads  to  the  regurgitation  of  blood  into  the  right  ventricle  under  the  cir- 
cumstances that  insufficiency  of  the  aortic  valve  allows  blood  to  flow 
back  into  the  left  ventricle.  As  a  result  of  this  leakage  the  right  ven- 
tricle becomes  hypertrophied.  If,  however,  the  leakage  becomes  too  great, 
dilatation  occurs  and  there  is  added  to  the  clinical  picture,  tricuspid 
insufficiency. 

Morbid  Anatomy. — When  the  pulmonary  valve  is  incompetent,  the 
structural  changes  are  usually  less  well  marked  than  those  encountered 
in  the  left  heart.  The  leaflets  are  less  thickened  and  the  sclerosis  of  the 
endocardium  is  less  markedly  evident.  Congenital  abnormalities,  prin- 
cipally in  the  form  of  an  increase  or  diminution  of  the  leaflets,  may  be 
the  cause  of  the  insufficiency.  As  a  rule,  these  abnormalities  are  unpro- 
ductive of  leakage. 

The  right  ventricle  is  generally  dilated  as  is  also  the  conus  arteriosus. 
The  viscera  show  changes  similar  to  those  occurring  from  failing  com- 
pensation in  other  cardiac  lesions. 

Functional  insufficiency  due  to  dilatation  of  the  pulmonary  artery 
and  valve  orifice  may  be  transient  or  permanent.  For  this  reason  pul- 
monary insufficiency  due  to  stretching  of  the  pulmonary  orifice  may  not 
be  demonstrable  until  post-mortem  unless  the  condition  is  permanent. 
Permanent  stretching  of  the  pulmonary  artery  is  encountered  most 
frequently  in  association  with  mitral  stenosis.  Testing  the  efficiency 
of  the  pulmonary  valve  by  pouring  water  into  the  artery  in  the  excised 
heart  and  measuring  the  diameter  of  the  pulmonary  orifice  are  of  doubt- 
ful value. 

Symptoms. — As  long  as  the  right  ventricle  compensates  for  the 
leakage  there  are  not  apt  to  be  any  symptoms.  If  other  valvular  lesions 
are  present,  the  symptoms  may  be  attributed  to  them  and  the  pulmonary 
trouble  overlooked  entirely.  Dyspnea,  especially  on  exertion,  is  perhaps 
the  most  common  symptom  and  this  may  be  paroxysmal  in  character. 
Owing  to  the   disturbance   of  the   pulmonary  circulation,  there  is  often 


.ENDOCARDITIS  695 

cough.     If  the  lesion  is  due  to  acute  endocarditis,  emboli  frequently  are' 
lodged  in  the  lungs.     In  such  cases  hemoptysis  is  common. 

In  cases  of  general  sepsis  the  pulmonary  valve  may  be  involved  alone 
or  in  association  with  valvular  lesions  elsewhere.  All  of  the  valvular 
areas  should  be  carefully  examined  in  the  presence  of  pyemic  symptoms. 

Physical  Signs. — Inspection. — Cyanosis  may  be  present.  The  apex 
beat  of  the  heart  is  displaced  downward  and  to  the  left.  Pulsation  is 
marked  in  the  epigastrium  due  to  the  lwpertrophied  right  ventricle  and 
in  the  second  and  third  interspaces  due  to  dilatation  of  the  conus  arte- 
riosus.    Jugular  pulsation  may  be  noted  also. 

Palpation. — Marked  pulsation  is  felt  in  the  second  and  third  inter- 
spaces to  the  left  of  the  sternum,  due  to  the  beating  of  the  conus  arterio- 
sus.    Rarely  a  diastolic  thrill  may  be  felt. 

Percussion. — The  transverse  diameter  of  cardiac  dulness  is  notice- 
ably increased. 

Auscultation. — The  murmur  of  pulmonary  insufficiency  is  diastolic 
in  time  and  usually  best  heard  at  the  second  costal  cartilage  on  the  left. 
The  punctum  maximum,  however,  may  be  midway  between  the  nipple 
and  the  sternum  (Bryant).  The  murmur  may  be  soft  and  of  brief 
duration  or  it  may  be  loud,  rough  and  replace  the  second  sound.  It 
sounds  more  superficial  than  the  diastolic  murmur  due  to  aortic  incom- 
petence. The  murmur  of  pulmonary  insufficiency  is  localized  or  slightly 
transmitted  down  the  left  border  of  the  sternum.  It  is  not  transmitted 
into  the  vessels  of  the  neck;  is  intensified  by  the  erect  posture;  and,  accord- 
ing to  Gerhardt,  is  intensified  by  expiration.  In  some  cases  the  vesicular 
murmur  may  be  jerky  in  character. 

Diagnosis. — Although  there  are  a  number  of  physical  signs  which 
are  said  to  be  more  or  less  distinctive  of  pulmonary  insufficiency,  the 
recognition  of  the  condition  is  fraught  with  difficulty.  It  is  to  be  dis- 
tinguished from  aortic  insufficiency  by  the  following  points:  A  diffuse 
rather  than  heaving,  forcible  cardiac  impulse;  absence  of  the  capillary 
and  water-hammer  pulses  and  large  arterial  pulse  pressure;  location 
of  murmur  to  the  left  of  the  sternum;  absence  of  transmission  into  the 
vessels  of  the  neck;  and  an  increase  in  the  intensity  of  the  murmur  during 
expiration. 

In  cases  of  mitral  stenosis  with  a  diastolic  murmur  to  the  left  of  the 
sternum  it  should  be  borne  in  mind  that  the  murmur  may  be  due  to 
dilatation  of  the  pulmonary  artery  rather  than  aortic  regurgitation. 
Cabot1  has  emphasized  the  frequency  with  which  a  diastolic  murmur 
to  the  left  of  the  sternum  occurs  in  association  with  mitral  stenosis. 
He  was  unable,  however,  to  demonstrate  at  autopsy  that  it  was  due  to 
dilatation  of  the  pulmonary  artery.  Its  differentiation  from  the  murmur 
of  aortic  regurgitation  will  depend  on  the  presence  or  absence  of  the 
arterial  phenomena  characteristic  of  the  latter  condition  (p.  674). 

PULMONARY  STENOSIS 

As  an  acquired  lesion  pulmonary  stenosis  is  exceedingl}'  rare,  but  as 
the  result  of  a  congenital  defect  is  relatively  common.  The  latter  will 
be  considered  under  congenital  lesions  of  the  heart. 

Etiology. — Acquired  disease  of  the  pulmonary  valves  may  be  the 
result  of  acute  rheumatic  fever  or  some  other  of  the  acute  infectious 
1  Trans.  Assoc.  Am.  Phys.,  1914. 


696  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

diseases  or  sclerotic  changes  which  lead  to  thickening  of  the  valve 
leaflets  and  later  to  atheromatous  degeneration.  Pulmonary  stenosis, 
whether  acquired  or  congenital,  seems  to  predispose  to  -pulmonary  tubercu- 
losis. Among  449  cases  of  pulmonary  stenosis  analyzed  by  Xorris,  tuber- 
culosis of  the  lungs  was  noted  in  160. 

Morbid  Anatomy. — The  changes  are  analogous  to  those  seen  in  the 
aortic  valve.  If  the  disease  is  acute,  vegetations  may  be  present  and  in 
some  instances  are  so  large  as  to  nearly  block  the  orifice.  In  other  in- 
stances the  inflammatory  process  is  evidently  chronic  in  nature  and 
structural  defects  result  from  induration,  thickening,  fusion,  or  cal- 
cification of  the  valve  leaflets.  The  conus  of  the  right  ventricle  is 
involved  in  a  large  proportion  of  cases.  In  addition  to  the  valvular 
defect,  hypertrophy  and  dilatation  of  the  right  auricle  and  ventricle  are 
usually  present.  With  the  onset  of  failing  compensation  tricuspid 
insufficiency  occurs  and  with  it  the  usual  phenomena  which  attend 
failing  compensation  in  other  cardiac  lesions. 

Pathological  Physiology. — The  partially  obstructed  pulmonary  orifice 
increases  the  work  of  the  right  ventricle  which  becomes  hypertrophied. 
If  the  stenosis  is  marked,  the  volume  of  blood  forced  into  the  pulmonary 
circulation  is  diminished.  This  leads  to  venous  stasis  and  the  marked 
cyanosis  which  is  characteristic  of  the  condition.  When  the  right  ven- 
tricle fails  to  compensate  for  the  defect,  dilatation  takes  place  and  with 
it  tricuspid  insufficiency. 

Symptoms. — The  acquired  form  does  not  give  rise  to  ver\>-  marked 
symptoms  so  long  as  the  compensation  is  maintained.  Varying  degrees 
of  shortness  of  breath  may  be  present  on  exertion.  Slight  cyanosis  and 
edema  may  be  present  but  are  usually  not  noted  until  tricuspid  insuffi- 
ciency occurs  and  compensation  fails. 

Physical  Signs. — Inspection. — Unless  failure  of  compensation  has 
occurred,  nothing  is  to  be  noted  on  inspection.  With  the  onset  of  failing 
compensation  the  evidences  of  venous  engorgement  which  follow  tricuspid 
insufficiency  will  be  seen.  Clubbing  of  the  fingers  is  not  often  present 
in  the  acquired  form. 

Palpation. — A  systolic  thrill  may  be  felt  in  the  second  and  third  inter- 
spaces to  the  left  of  the  sternum. 

Percussion. — Cardiac  clulness  is  increased  to  the  right  of  the  sternum 
as  the  result  of  hypertrophy  or  dilatation  or  both,  of  the  right  ventricle. 

Auscultation. — The  characteristic  feature  is  the  presence  of  a  murmur 
systolic  in  time  and  best  heard  at  the  pulmonary  area.  It  is  usually  trans- 
mitted upward  and  to  the  left  toward  the  clavicle.  The  murmur  is 
usually  harsh  in  character  and  gives  the  impression  of  being  superficially 
placed.  The  second  pulmonic  sound  is  either  very  feeble  or  entirely 
absent.  If  pulmonary  insufficiency  is  also  present,  the  second  pulmonic 
sound  may  be  replaced  by  a  diastolic  murmur. 

Diagnosis. — Acquired  pulmonary  stenosis  is  so  exceedingly  rare  that 
a  diagnosis  of  the  condition  is  permissible  only  when  every  means  has 
been  taken  to  determine  the  source  of  the  murmur.  It  is  to  be  borne  in 
mind  that  systolic  murmurs  heard  at  the  pulmonary  area  are  extremely 
common.  In  the  great  majority  of  instances  they  are  functional  in  char- 
acter but  occasionally  are  due  to  organic  lesions  situated  elsewhere. 

Not  infrequently  the  murmur  of  aortic  stenosis  is  best  heard  to  the 
left  of  the  sternum.     In  such  cases  the  pulmonic  second  sound  is  either 


ENDOCARDITIS  697 

normal  or  accentuated  instead  of  being  absent  or  very  faint.  The  mur- 
mur of  aortic  stenosis  is  transmitted  to  the  vessels  of  the  neck  while  that 
of  pulmonary  stenosis  is  not. 

Recently  Oille,  Graham  and  Detweiler1  have  called  attention  to  the 
fact  that  systolic  murmurs  at  the  pulmonary  area  are  not  infrequently 
due  to  mitral  insufficiency.  In  such  cases  there  is  no  murmur  at  the 
apex.  Even  when  a  systolic  murmur  due  to  mitral  insufficiency  is  heard 
at  the  apex  it  is  often  loudest  at  the  pulmonary  area  over  the  left 
auricular  appendage  (see  Fig.  163).  Rarely  a  loud  systolic  murmur  due 
to  a  patent  ductus  arteriosus  is  heard  to  the  left  of  the  sternum.  This 
will  be  referred  to  under  congenital  heart  lesions. 

Functional  murmurs,  systolic  in  time  and  best  heard  at  the  pulmonary 
artery  may  be  present  in  any  condition  associated  with  anemia.  Often 
a  transient  systolic  murmur  is  heard  when  the  heart  is  overacting  as  the 
result  of  nervousness  or  exertion. 

Just  as  in  the  case  of  aortic  stenosis,  the  character  of  the  second  sound 
is  the  important  feature.  If  true  stenosis  is  present  the  second  sound  is 
feeble  or  absent;  in  all  other  instances,  it  is  normal  or  accentuated. 

1  Jour.  Am.-  Med.  Assoc,  Oct.  2,  1915. 


CHAPTER.  XXVIII 
CONGENITAL  HEART  DISEASE 

"Congenital  cardiac  disease  may  be  defined  as  that  condition  in 
which,  through  arrest  of  development  or  disease  occurring  in  intrauterine 
life,  anomalies  in  the  anatomical  structure  of  the  heart  or  great  vessels 
exist,  leading  to  irregularities  in  the  circulation.  It  is  frequently  associ- 
ated with -congenital  cyanosis  and  clubbing  of  the  fingers,  and  constitutes 
in  extreme  cases  the  morbus  coeruleus  of  the  older  writers"  (Maude 
E.  Abbott). 

For  the  most  part  congenital  lesions  of  the  heart  are  of  pathological 
interest  only.  In  some  instances  the  defect  is  so  great  as  to  be  incom- 
patible with  life;  in  others,  the  individual  may  reach  adult  life  without 
there  being  any  evidence  of  cardiac  trouble,  or  there  may  be  distinctive 
symptoms;  in  still  others,  the  defect  may  consist  of  some  abnormality 
from  which  there  is  no  disturbance  of  function  whatever,  as  for  instance 
the  presence  of  four  or  of  two  leaflets  in  the  aortic  or  pulmonary  valves. 
Supernumerary  leaflets  occur  more  frequently  in  the  pulmonary  valve 
than  the  aortic  while  the  presence  of  two  instead  of  three  leaflets  occurs 
more  often  in  the  latter  (19  out  of  21  cases  observed  by  Osier). 

The  chief  clinical  interest  in  congenital  defects,  which  are  not  incom- 
patible with  life,  is  that  they  seem  extremely  prone  to  become  the  seat 
of  an  acute  endocarditis  or,  as  in  the  case  of  anomalous  valves,  to  become 
the  seat  of  sclerotic  changes. 

The  best  presentations  of  the  subject  are  those  of  Maude  E.  Abbott1 
and  Lawrence  Humphry.2  Only  the  more  common  defects  will  be  con- 
sidered here. 

Symptoms  of  Congenital  Heart  Disease. — Symptoms  may  be  present 
from  birth  or  they  may  not  appear  until  the  child  is  a  year  or  more  old. 
The  first  symptom  to  be  noted  is  cyanosis  which  is  present  in  about  90 
per  cent,  of  the  cases.  This  symptom  is  so  characteristic  of  congenital 
disease  of  the  heart  that  the  terms  "blue  disease  "  and  "morbus  cseruleus" 
are  synonymous.  The  cyanosis  is  most  noticeable  in  the  face,  hands  and 
feet  which  are  of  a  livid  or  bluish  tint.  Usually  the  cyanosis  is  most 
marked  in  the  nose,  ears,  lips  and  the  tips  of  the  fingers  and  toes.  The 
mucous  membranes  may  present  a  cyanotic  tinge  also.  The  cause  of 
the  cyanosis  is  not  altogether  clear  and  various  hypotheses  have  been 
advanced.  It  has  been  suggested  that  the  condition  is  caused  by:  (1) 
The  mixture  of  venous  and  arterial  blood;  (2)  to  deficient  aeration  of  the 
blood;  and  (3)  general  venous  congestion.  The  latter  view  is  the  one 
most  generally  held,  although  it  cannot  be  said  to  cover  all  cases.  There 
are  not  a  few  instances  in  which  no  satisfactory  explanation  is  forth- 
coming. Associated  with  the  cyanosis  there  is  often  a  marked  poly- 
cythemia.    The  red  cells  may  be  as  high  as  11,000,000  per  cubic  mil- 

1  Osler's  "Modern  Medicine,"  vol.  iv,  1st  ed. 

2  Allbtjtt  and  Rollestox:  "System  of  Medicine,"  vol.  vi. 

698 


CONGENITAL    HEART    DISEASE  699 

limeter.  In  addition  to  the  high  red  cell  count  the  percentage  of 
hemoglobin  is  increased  and  the  specific  gravity  of  the  blood  is  ab- 
normally high.     Hemorrhages  sometimes  occur. 

Clubbing  of  the  fingers,  usually  of  an  extreme  degree,  is  a  very  fre- 
quent manifestation.  Clubbing  of  the  fingers  and  cyanosis  in  a  small 
child  are  of  themselves  sufficient  evidence  upon  which  to  base  a  diagnosis 
of  congenital  heart  disease  (see  Fig.  1).  Dyspnea  may  be  a  marked  fea- 
ture; it  may  occur  only  as  the  result  of  overexertion  or  it  may  be 
paroxysmal  in  character.  Cough  may  be  present  and  is  apt  to  be 
brought  on  or  increased  by  exertion. 

The  surface  temperature  is  usually  low  and  this  is  especially  noticeable 
in  the  hands  and  feet.  In  the  majority  of  cases  of  congenital  disease  the 
child  is  weakly  and  succumbs  early  in  life.  In  those  who  reach  adult  life, 
stenosis  of  the  pulmonary  orifice  is  the  lesion  most  frequently  present. 

In  many  cases  the  physical  signs  are  marked,  especially  the  presence 
of  a  murmur.  The  existence  of  the  latter  in  association  with  one  or 
more  of  the  characteristic  symptoms  renders  the  diagnosis  of  congenital 
disease  easy,  although  it  may  be  difficult  and  often  impossible  to  deter- 
mine the  exact  nature  of  the  defect. 

Congenital  Pulmonary  Stenosis  and  Atresia  of  the  Pulmonary  Artery. 
— Stenosis  of  the  pulmonary  orifice  acquired  in  adult  life  is  exceedingly 
rare.  Congenital  stenosis,  on  the  other  hand,  is  relatively  common.  It 
may  be  the  result  of  fetal  endocarditis  or  of  anomalies  in  the  development 
of  the  heart.  Of  366  cases  of  congenital  lesions  reported  by  Peacock  and 
Keith  254,  or  69  per  cent.,  were  due  to  pulmonary  stenosis. 

The  obstruction  may  be  due:  (1)  To  constriction  of  the  orifice,  with  or 
without  atresia  or  obliteration  of  the  artery;  (2)  to  obliteration  or  narrow- 
ing of  the  pulmonary  artery:  and  (3)  to  stenosis  of  the  conus  arteriosus. 
In  the  majority  of  cases  the  stenosis  is  associated  with  other  developmen- 
tal anomalies  the  most  frequent  of  which  are  patency  of  the  foramen 
ovale  and  ductus  arteriosus,  an  opening  in  the  ventricular  septum  and 
transposition  or  malposition  of  the  aorta  and  pulmonary  artery. 

Symptoms  and  Physical  Signs. — The  two  distinctive  features  are 
cyanosis  and  clubbing  of  the  fingers  and  toes.  In  addition  there  are 
dyspnea,  especially  on  exertion,  inertia  and  a  tendency  to  chilliness.  If 
the  child  passes  the  period  of  infancy,  its  growth  is  usually  retarded. 

On  examination,  the  precordium  is  usually  seen  to  be  rather  prominent 
and  the  cardiac  impulse  heaving  and  diffuse  in  character.  In  those  cases 
in  which  the  cyanosis  is  marked,  the  retinal  vessels  may  be  tortuous  and 
their  lumen  irregular,  being  in  some  places  very  wide  and  in  other  places 
veiy  narrow.  A  systolic  thrill  may  be  felt  over  the  base  of  the  heart  to 
the  left  of  the  sternum.  Percussion  shows  the  transverse  area  of  cardiac 
dulness  to  be  increased,  especially  to  the  right  of  the  sternum.  On  aus- 
cultation a  loud,  harsh  systolic  murmur  may  be  perceptible  over  the  whole 
heart  but  with  its  maximum  intensity  at  the  pulmonary  area.  The  mur- 
mur may  be  localized  or  heard  only  at  the  pulmonary  area.  The  second 
pulmonic  sound  is  feeble  or  absent. 

The  differentiation  of  this  murmur  from  other  systolic  murmurs  heard 
at  the  pulmonary  area  has  been  considered  under  acquired  pulmonary 
stenosis. 

Patent  Foramen  Ovale. — During  fetal  life  there  is  normally  an  open- 
ing in  the  interauricular  septum,  known  as  the  foramen  ovale.     Shortly 


700 


DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


after  birth  this  opening  closes.  In  some  instances,  however,  the  opening 
persists  and  allows  of  the  passage  of  blood  from  one  auricle  to  the  other 
(see  Fig.  390) ;  not  infrequently  the  opening  persists  but  does  not  allow  of 
leakage  (see  Fig.  391).  In  the  great  majority  of  cases,  in  which  after 
death  a  small  probe  can  be  passed  through  the  foramen,  the  condition  is 
not  to  be  looked  upon  as  abnormal. 


Fig.  390. — Patulousbut  incompetent  foramen  ovale.    (Pennsylvania  Hospital.) 

If,  however,  the  opening  is  widely  dilated  it  may  be  considered  as  being- 
anomalous  and  in  such  cases  serious  disturbances  in  the  circulation  are  apt 
to  occur.  The  fact  that  the  channel  runs  obliquely  through  the  auricular 
septum,  and  that,  therefore,  the  openings  on  the  two  sides  are  not  directly 
opposite  to  each  other,  favors  competency.  A  demonstrable  opening  was 
recorded  in  only  86  cases  among  8640  autopsies  (0.9  per  cent.)  at  the  Phila- 
delphia General  Hospital  (Norris). 

Patency  of  the  foramen  ovale  may  occur  alone  but  it  is  frequently 
associated  with  other  defects  and  particularly  with  pulmonary  stenosis. 


CONGENITAL    HEART    DISEASE  701 

Symptoms  and  Physical  Signs. — Small  openings  are  not  apt  to  give 
rise  to  either  signs  or  symptoms  and  even  a  wide  opening  (see  Fig.  397) 
may  exist  without  manifesting  itself  during  life.     In  a  well-marked  case 


Fig.  391. — Patulous  foramen  ovale.  Heart  of  a  woman  aged  seventy  years,  who  died 
of  croupous  pneumonia,  having  advanced  general  arteriosclerosis.  The  illustration  shows 
a  chronic,  more  or  less  diffuse,  mitral  thickening,  with  contraction  of  the  chordea?  tendinese, 
and  marked  hypertrophy  of  the  left  ventricle.  The  foramen  ovale  is  quite  large  and  patu- 
lous, but  owing  to  its  oblique  course  it  was  probably  functionally  competent. 

the  symptoms  may  be  those  of  congenital   disease,  namely,  cyanosis, 
dyspnea,  often  paroxysmal  in  character,  cold  extremities,  inertia,  etc. 
The  murmur  may  be  systolic,  diastolic  or  presystolic  in  time  and  is 


702  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

best  heard  in  the  third  interspace  to  the  left  and  close  to  the  sternum. 
If  cyanosis  is  present  constantly  or  only  intermittently,  a  patent  foramen 
ovale  may  be  suspected  as  the  cause  of  the  murmur.  Tortuosity  and  in- 
equalities of  the  retinal  vessels  may  be  present. 


Fig.  392. — Patulous  interventricular  septum  with  acute  endocarditis.  In  the  septum 
ventriculorum,  just  to  the  left  of  the  beginning  of  the  conus  arteriosus,  there  is  an  oval 
opening,  3.5  X  2.5  cm.  in  diameter,  which  appears  as  a  funnel-shaped  excavation  in  the 
ventricular  septum.  The  opening  into  the  left  ventricle  is  nearly  closed  by  large  wart-like 
vegetations.  These  vegetations  extend  from  the  opening  upward  into  the  conus  arteriosus 
and  are  continuous  with  those  in  the  right  anterior  leaflet  of  the  pulmonary  valve. 

Imperforate  Ventricular  Septum. — A  very  common  congenital  defect 
is  an  abnormal  communication  between  the  two  ventricles.     The  perfora- 


CONGENITAL    HEART   DISEASE  703 

tion  usually  occurs  just  beneath  the  aortic  orifice,  in  the  membranous 
or  undefended  space,  so-called  because  normally  the  septum  here  consists 
of  two  layers  of  endocardium.  In  the  majority  of  instances  this  defect 
occurs  in  association  with  other  anomalies.  In  78  per  cent,  of  Abbott's 
cases  it  appeared  in  combination  with  other  defects;  most  commonly  with 
pulmonary  stenosis.  In  addition  to  causing  serious  alterations  in  the  cir- 
culation, these  perforations  often  become  the  site  of  an  acute  endocarditis 
(see  Fig.  392).  The  effect  of  an  imperforate  septum  upon  the  circulation 
and  upon  the  heart  depends  on  whether  it  exists  alone  or  in  association 
with  other  defects.  When  it  occurs  alone,  it  produces  hypertrophy  of 
both  ventricles. 

Symptoms  and  Physical  Signs.- — The  symptoms  will  depend  on 
whether  the  condition  occurs  as  an  isolated  lesion  or  whether  it  is  associated 
with  other  defects.  In  the  latter  case  the  predominant  symptoms  may 
be  due  to  the  associated  lesion  of  which  pulmonary  stenosis  is  the 
commonest.  When  the  lesion  exists  alone  the  symptoms  are  rarely 
marked  and  may  consist  of  dyspnea  and  in  some  cases  transient  attacks  of 
cyanosis  on  exertion. 

This  is  one  of  the  congenital  defects  in  which  the  character  of  the  mur- 
mur may  enable  one  to  arrive  at  a  correct  diagnosis.  The  murmur  was 
first  described  by  Roger  in  1879  and  is  often  referred  to  as  the  bruit  de 
Roger.  It  is  usually  loud  and  harsh  and  best  heard  in  the  third  interspace 
to  the  left  of  the  sternum  or  to  the  left  of  the  xiphoid  cartilage.  It  is 
fixed  and  is  not  transmitted  as  is  the  case  with  organic  valvular  murmurs. 
The  characteristic  feature  of  the  murmur  is  its  length.  It  commences 
early  in  systole  and  is  prolonged  into  diastole  so  that  it  obscures  the  second 
sound  entirely.  Roger  in  his  original  description  states  that  "the  mur- 
mur corresponds  with  a  very  extensive  thrill  which  exactly  coincides  with 
it."  At  the  base  of  the  heart  the  second  pulmonic  sound  is  accentuated. 
The  diagnosis  rests  on  the  hearing  of  a  loud,  continuous  murmur  with  no 
interval  between  the  systolic  and  diastolic  portions  to  the  left  of  the 
sternum. 

Patent  Ductus  Arteriosus  (Botalli). — The  ductus  arteriosus  is  an 
essential  component  of  the  fetal  circulatory  apparatus.  It  is  a  short 
thick  trunk  connecting  the  left  branch  of  the  pulmonary  artery  with  the 
aorta  and  serves  to  carry  the  unaerated  blood  from  the  head  and  upper 
extremities  to  the  descending  aorta,  and  thence  to  the  placenta.  At 
birth  it  quickly  ceases  to  be  used  and  becomes  impermeable  about  the  third 
week.  It  is  finally  transformed  into  the  ligamentum  arteriosum.  Just 
as  in  the  case  of  the  foramen  ovale  the  duct  may  remain  patent  and  as  a 
result  may  or  may  not  lead  to  circulatory  disturbances.  Patency  of  the 
duct  may  be  the  only  anomaly  present  but  more  commonly  it  is  associated 
with  other  defects,  namely,  pulmonary  stenosis,  transposition  of  the  great 
vessels  (see  Fig.  393)  or  stenosis  of  the  aorta  (see  Fig.  39-4).  Among  106 
instances  of  patency  of  the  duct  Abbott  found  but  19  in  which  the  lesion 
occurred  alone.  Goodman1  collected  71  cases,  34  of  which  were  autopsied 
and  the  remainder  were  clinical  observations.  Recently  Stoddard2  has 
added  22  additional  cases. 

Hypertrophy  with  or  without  dilatation  of  the  right  ventricle  is 
a  constant  finding  in  adult  cases. 

1  Univ.  Pa.  Med.  Bull,  December,  1910. 

2  Arch.  Int.  Med.,  July,  1915. 


704  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

Symptoms  and  Physical  Signs. — In  uncomplicated  cases  the  symptoms 
are,  as  a  rule,  not  striking,  and  may  be  wanting  entirely.  Cyanosis 
and  clubbing  of  the  fingers,  so  commonly  seen  in  other  congenital  affec- 
tions, are  unusual.     Dyspnea  and   palpitation  on  exertion  may  occur. 

The  diagnosis  depends,  almost  entirely,  on  the  physical  signs,  of 
which  the  murmur  is  the  most  important.  The  murmur  is  produced 
by  the  rush  of  blood  through  the  duct  from  the  aorta  to  the  pulmonary 
artery.     Its  point  of  maximum  intensity  is  in  the  second  left  interspace. 


Fig.  393. — Patent  ductus  arteriosus.  Transposition  of  the  aorta  and  the  pulmonary 
artery;  patent  ductus  arteriosus;  hypertrophy  of  the  right  ventricle.  Patent  foramen 
ovale;  partial  atelectasis  of  the  right  lung;  general  visceral  congestion.     (A.  G.  Ellis.) 

The  murmur  is  usually  loud,  harsh,  and  of  a  churning  or  rasping  quality. 
As  in  the  case  of  imperforate  ventricular  septum  the  murmur  is  very  long 
beginning  in  systole  and  continuing  into  diastole.  It  may  be  loudest  at 
its  commencement  and  gradually  diminish  or  it  may  gradually  become 
intense  at  the  middle  period  and  then  wane.  In  other  instances  the  mur- 
mur may  be  double  or  while  continuous  may  have  a  systolic  and  a  dias- 
tolic accentuation.     The  second  pulmonic  sound  is  usually  much  accen- 


CONGENITAL    HEART    DISEASE 


705 


Pulmonary 
artery 


Descend- 
ing aorta 


Fig.  394. — Congenital  aortic  stenosis  with  patency  of  the  ductus  arteriosus.  Patho- 
logic Notes:  The  aorta  is  very  small,  measuring  at  the  arch  only  4.5  cm.  in  diameter, 
while  the  pulmonary  artery  is  twice  this  size.  The  innominate,  left  vertebral,  and  sub- 
clavian arteries  are  normal  in  position  and  size.  Immediately  at  the  junction  of  the  lower 
edge  of  the  left  subclavin  artery  and  the  aorta,  the  latter  vessel  shows  a  sudden  and  marked 
constriction,  the  external  diameter  of  which  measures  12  mm.,  while  3  cm.  above  and  below 
the  constriction  the  aorta  measures  2  and  2.5  cm.  in  diameter.  On  opening  the  aorta  and 
looking  down  toward  the  constriction  the  vessel  appears  to  end  in  a  smooth,  rounded,  blind 
pouch,  but  on  closer  inspection  a  pinhead-sized  opening  can  be  seen,  through  which  a  small 
probe  can  be  passed.     {Pennsylvania  Hospital.) 


45 


706  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

tuated,  a  point  which  serves  to  distinguish  the  murmur  from  that  caused 
by  pulmonary  stenosis.  The  murmur  is  transmitted  upward  along  the  left- 
margin  of  the  sternum  into  the  left  carotid.  It  is  also  well  heard  pos- 
teriorly in  the  left  interscapular  region,  being  loudest  during  expiration. 

A  systolic  thrill  is  often  felt  at  the  base  of  the  heart  to  the  left;  the 
thrill  may  be  felt  throughout  the  cardiac  cycle. 

Gerhardt,  in  1867,  called  attention  to  the  presence  of  dilatation  of 
the  pulmonary  artery  in  these  cases.  This  is  recognized  by  the  presence 
of  systolic  pulsation  in  the  second  left  interspace,  due  to  forcible  closure 
of  the  pulmonary  valves,  and  an  extension  of  dulness  in  the  first  second 
interspaces  to  the  left  of  the  sternum.  Dilatation  of  the  pulmonary 
arterjT  may  be  determined  also  by  the  use  of  the  fluoroscope  or  X-ray 
plate.  In  a  case  now  under  my  observation  the  occurrence  of  a  loud 
rasping  murmur,  best  heard  in  the  second  left  interspace,  and  the  presence 
of  a  shadow  in  the  X-ray  plate  indicating  dilatation  of  the  pulmonary 
artery,  point  toward  a  patent  ductus  arteriosus.  The  value  of  the 
X-rays  in  these  cases,  however,  is  not  yet  established.  Stoddard1 
states  that  only  two  cases  showing  a  dilated  pulmonary  artery  with 
roentgenoscopy  have  been  confirmed  by  autopsy. 

Dextrocardia.- — This  term  is  applied  to  the  condition  in  which  the 
heart  is  on  the  right  side  instead  of  the  left.  Two  varieties  of  dextrocardia 
are  to  be  recognized:  (1)  True  dextrocardia  which  is  a  congenital  anomaly 
and  is  the  result  of  transposition  of  the  viscera.  Complete  transposition 
of  the  viscera,  a  condition  in  which  the  heart,  stomach  and  spleen  are 
on  the  right  side  and  the  liver  on  the  left,  is  not  excessively  rare.  Com- 
plete transposition  of  the  viscera  interferes  in  no  way  with  the  normal 
functions  and  is  usually  discovered  accidentally  during  a  routine  ex- 
amination. It  has  no  clinical  significance.  Transposition  of  the  heart 
alone  may  occur  but  is  very  rare  (2  out  of  412  congenital  affections 
collected  by  Abbott).  In  such  cases  there  may  be  a  disarrangement  of 
the  great  vessels  with  symptoms  of  congenital  disease. 

2.  Pseudo-dextrocardia  max  be  used  to  designate  those  cases  in  which 
the  heart  is  displaced  to  the  right  but  not  transposed.  It  occurs  when- 
ever there  is  a  large  left-sided  pleural  effusion  which  pushes  the  heart 
and  mediastinal  contents  to  the  right.  Displacement  of  the  heart 
to  right  is  often  very  marked  when  there  is  present  extensive  fibroid 
disease  of  the  right  lung.  In  such  cases  the  retraction  of  the  fibroid 
tissue  draws  the  heart  and  mediastinal  contents  to  the  right.  The 
retraction  and  diminution  in  size  of  the  right  chest  which  ensues 
tends  to  emphasize  the  displacement  of  the  heart  (see  Fig.  28). 

Fishberg2  has  called  attention  to  the  frequency  of  acquired  or  pseudo- 
dextrocardia  in  cases  of  tuberculosis,  especially  in  the  advanced  stage. 
He  finds  that  the  heart  is  not  only  displaced  but  slightly  rotated  on  its 
vertical  axis.  This  tends  to  bring  the  base  of  the  heart  closer  to  the 
chest  wall  and  push  or  pull  the  apex  away  from  it. 

It  is  to  be  borne  in  mind  that  displacement  of  the  heart  is  entirely 
different  from  transposition.  In  the  latter  the  heart  occupies  the  same 
position  in  the  right  chest  that  it  normally  does  in  the  left.  In  cases 
of  displacement  the  heart  maintains  its  normal  relationship  but  is  pushed 
or  pulled  to  the  right  although  in  cases  of  effusion  the  apex  beat  may  be 

1  Loc.  cit. 

2  Arch.  Int.  Med.,  April,  1914. 


CONGENITAL    HEART    DISEASE  707 

displaced  upward.  To  speak  of  the  apex  beat  being  seen  or  felt  in  one 
of  the  interspaces  to  the  right  of  the  sternum  in  cases  of  displacement,  is 
an  error.  What  is  mistaken  for  the  apex  beat  is  the  pulsation  of  the  right 
ventricle  which  has  been  pushed  over  by  an  effusion  or  pulled  over,  and  at 
the  same  time  exposed,  by  the  retraction  of  the  fibroid  lung. 


CHAPTER   XXIX 
ANGINA  PECTORIS 

There  is  considerable  uncertainty  as  to  the  proper  classification 
of  the  various  painful  sensations  centering  about  the  precordium. 
There  are  two  types  concerning  which  most  observers  are  in  agreement: 

(1)  True  angina  pectoris  which  is  usually  associated  with  disease  of  the 
coronary  arteries  and  which,  in  the  great  majority  of  cases,  is   fatal. 

(2)  Precordial  pain  which  is  due  to  disturbed  function;  is  lacking  either 
the  intensity  or  the  distribution  of  true  anginal  pain;  is  not  associated 
with  disease  of  the  coronary  arteries  or  the  heart;  and  is  never  fatal. 
In  this  group  may  be  placed  those  instances  of  heart  pain  occurring 
in  neurotic,  emotional  women  and  in  those  addicted  to  the  excessive 
use  of  tea,  coffee  or  tobacco.  Pain  due  to  the  excessive  use  of  tobacco 
is  not  common.  It  may  be  very  severe.  Attacks  of  pain  due  to  this 
cause  are  prolonged,  as  compared  to  true  angina.  Painful  sensations 
arising  under  these  circumstances  are  often  referred  to  as  pseudo-angina 
or  angina  pectoris  vasomotoria. 

In  addition  to  these  two  groups,  which  are,  as  a  rule,  readily  differ- 
entiated, there  is  a  third  group  which  may  be  termed  incipient  angina 
pectoris  major.  In  this  form  of  the  disease  there  may  be  nothing  more 
than  a  sense  of  oppression  about  the  heart  or  if  pain  does  occur  it  is 
not  severe  nor  does  it  radiate.  Many  deny  to  these  lighter  attacks  the 
name  angina  pectoris.  There  can  be  no  question,  however,  that  they  are 
often  the  forerunners  of  true  angina  and  that  as  time  goes  on  the  attacks 
tend  to  become  more  and  more  severe  until  they  finally  manifest  all  the 
characteristics  of  the  major  form  of  the  disease. 

Symptoms  of  incipient  angina  pectoris  are  especially  apt  to  occur 
m  patients  suffering  from  one  of  two  conditions,  namely,  arterial  hyper- 
tension or  aortitis,  especially  the  syphilitic  form  of  the  disease.  The 
importance  of  this  group  cannot  be  overestimated  because  a  correct 
interpretation  of  the  pain  enables  us  to  institute  treatment  which  will 
either  cure  the  trouble  or  at  least  mitigate  the  symptoms  and  prolong 
the  patient's  life. 

ANGINA  PECTORIS  MAJOR 

Etiology. — In  the  great  majority  of  cases  true  angina  pectoris  is  one 
of  the  manifestations  of  a  general  arterio-sclerosis,  an  organic  heart 
lesion,  or  both;  the  etiological  factors  are,  therefore,  essentially  the  same. 

The  disease  is  encountered  most  frequently  between  the  ages  of 
forty  and  seventy,  the  highest  incidence  being  in  the  fifth  and  sixth  dec- 
ades. When  true  angina  occurs  in  an  individual  under  forty  years  of 
age,  syphilis  is  the  most  probable  cause. 

Although  degenerative  changes  in  the  arteries  occur  in  all  walks  of 
life  and  are  often  encountered  in  their  most  severe  form  among  the  work- 
ing classes,  angina  pectoris  is  rarely  encountered  among  these  people. 

708 


ANGINA    PECTORIS  709 

It  would  seem  that  in  addition  to  the  arterial  changes  other  factors  are 
necessary,  namely,  worry  and  the  strain  and  stress  of  high-pressure  living. 
Certain  it  is  that  the  vast  majority  of  cases  of  angina  pectoris  major  are 
met  with  among  those  engaged  in  pursuits  entailing  much  responsibility 
and  in  whom  the  mental  strain  is  great.  Furthermore,  in  not  a  few 
instances  such  individuals  increase  their  liability  to  the  disease  by 
reason  of  overindulgence  in  eating,  in  drinking  and  in  the  excessive  use  of 
tobacco. 

It  has  been  frequently  commented  that  members  of  the  medical  pro- 
fession seem  to  be  especially  liable  to  this  affection.  In  a  series  of  268 
cases  Osier  states  that  no  less  than  33  were  physicians. 

While  angina  pectoris  does  occur  in  women,  it  is  relatively  infrequent. 

Occasionally  families  are  encountered  in  which  there  is  apparently  a 
predisposition  to  arterio-sclerosis  which  terminates  in  a  fatal  attack  of 
angina  pectoris.  In  a  family  under  the  care  of  one  of  us  (Norris)  no  less 
than  five  brothers  and  sisters  have  died  in  this  way.  The  disease  has 
been  noted  as  occurring  in  the  members  of  three  successive  generations. 

Morbid  Anatomy. — Hoover  classifies  the  anatomical  lesions  in  true 
angina  as  follows: 

1.  Isolated  disease  of  the  coronary  arteries  unassociated  with  any 
affection  of  the  aorta,  aortic  valves,  or  systemic  arteries. 

2.  Disease  of  the  coronary  arteries  associated  with  systemic  arterial 
disease. 

3.  Partial  or  complete  occlusion  of  the  lumen  of  the  coronary  arteries 
at  their  origin  on  account  of  disease  of  the  aortic  valves  or  disease  of  the 
root  of  the  aorta.  (Allbutt  believes  all  cases  of  angina  to  be  associated 
with  disease  of  the  aorta.) 

4.  Absence  of  disease  of  the  vessels  and  heart,  the  vascular  crises  being 
due  to  arterial  spasm,  the  result  of  vasomotor  disturbances. 

Finally,  it  should  be  mentioned  that  in  some  cases  one  of  the  coronaries 
may  be  blocked  by  a  thrombus  or  embolus. 

Arterio-sclerosis  of  the  coronary  arteries  is  by  common  consent  ac- 
cepted as  the  pathologic  basis  of  anginal  seizures.  The  radiation  of  pain 
to  the  chest,  neck  and  arms  is  apparently  a  segmental  phenomenon  due  to 
radiation  and  transference  of  pain  to  the  periphery  from  those  segments 
of  the  cord  which  receive  impulses  from  the  heart  (third  cervical  to  third 
dorsal)  (see  "Zones  of  Cutaneous  Hyperesthesia,"  Figs.  42  and  43). 

In  seeking  for  an  explanation  as  to  the  mechanism  of  the  phenomena 
which  characterizes  angina  pectoris  the  intermittent  claudication  hypothesis 
is  most  in  favor.  We  know,  for  instance,  that  a  restricted  blood  supply  is 
a  recognized  cause  of  cramp  in  the  muscles  and  that  if  the  muscles  are  not 
properly  irrigated  and  waste  products  removed,  exhaustion  with  or  with- 
out pain  is  likely  to  ensue.  The  most  familiar  clinical  example  of  this  is 
the  condition  known  as  intermittent  claudication,  in  which,  as  a  result  of 
narrowing  of  the  arteries  of  the  legs,  pain  develops  if  the  patient  overexerts 
himself  either  by  walking  too  fast  or  too  far.  In  old  people  whoso 
arteries  have  undergone  degenerative  changes,  severe  cramps  in  the  legs 
or  thighs  are  sometimes  induced  by  walking;  in  other  instances,  the  con- 
dition manifests  itself  by  extreme  fatigue  of  the  leg  muscles.  So  long  as 
the  patient  keeps  relatively  quiet,  the  diseased  vessels  are  capable  of  fur- 
nishing an  adequate  supply  of  blood,  but  if  extra  demands  are  made  on  the 
muscles  more  blood  is  needed  and  this  the  damaged  arteries  cannot  supply. 


710  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

The  result  is  a  local  anemia  with  impairment  or  loss  of  function  and  often 
severe  pain. 

The  constricting  effect  of  diseased  vessels  as  a  cause  of  failure  of  power, 
with  or  without  pain,  in  muscles  during  action  was  first  suggested  by- 
Allan  Burns  in  1809.  In  support  of  this  contention  Burns  showed  that  if 
a  ligature  be  applied  to  a  limb  with  moderate  tightness  enough  blood  is 
admitted  to  the  muscles  for  the  performance  of  quiet  work,  but  if  vigorous 
action  is  attempted  the  muscles  quickly  become  fatigued  and  severe  pain 
is  apt  to  occur. 

It  is  thus  apparent  that  the  vascular  crisis  which  characterizes  angina 
pectoris  has  much  in  common  with  that  occurring  in  intermittent  clau- 
dication. If  the  function  of  the  coronary  arteries  has  become  impaired 
either  as  the  result  of  partial  occlusion  of  their  openings  or  as  the  result  of 
an  endarteritis  the  blood  supply  to  the  heart  is  limited  although  it  may  be 
sufficient  providing  undue  demands  are  not  made  upon  the  organ. 

Furthermore,  it  is  known  that  angina  attacks  are  usually  precipitated 
by  walking  too  fast,  by  walking  against  the  wind  or  by  some  other  form  of 
overexertion.  In  addition  sudden  emotion,  particularly  anger,  is  apt  to 
cause  a  seizure.  Whether  because  of  exertion  or  anger  the  heart  is  over- 
taxed by  the  suddenly  increased  bloocl-pressure,  the  arteries  are  unable  to 
supply  the  extra  amount  of  blood  demanded  and  as  a  result  pain,  syncope 
or  even  sudden  death  are  produced. 

In  those  instances  in  which  the  coronary  arteries  are  free  from  disease 
the  only  plausible  explanation  is  that  the  anginal  seizure  is  caused  by  a 
spasm  of  the  arteries.  This  hypothesis  is  supported  by  the  fact  that  pain 
or  disturbance  of  function  are  produced  by  arterial  spasm  in  other  parts 
of  the  body.  Intermittent  claudication,  for  instance,  may  be  due  either 
to  an  endarteritis  or  to  spasm  of  a  healthy  artery.  In  the  same  category 
are  to  be  placed  transient  attacks  of  aphasia  and  transient  amaurosis.  In 
the  latter  instance  it  is  possible  to  see  the  spasm  of  the  retinal  arteries  by 
means  of  the  ophthalmoscope. 

There  are  few  who  support  the  hypothesis  that  the  phenomena  of 
angina  pectoris  may  be  caused  by  neuralgia  either  central  or  originating 
in  the  gray  matter  of  the  cord  or  cardiac  ganglia  or  that  they  arise  as  the 
result  of  a  neuritis  of  the  cardiac  nerves. 

Symptoms. — While  an  attack  of  angina  pectoris  is  always  a  menace  to 
the  patient's  life,  it  is  a  mistake  to  assume  that  a  fatal  termination  is  the 
rule  after  a  single  or  even  two  or  three  seizures.  It  is  to  be  borne  in  mind 
that  the  attacks  manifest  themselves  in  varying  degrees  of  severity  and 
that  seizures  of  true  angina  pectoris  may  occur  at  irregular  intervals  over 
along  period  of  years. 

Although  angina  pectoris  major  sooner  or  later  ends  fatally,  in  the  vast 
majority  of  cases,  complete  recovery  has  been  noted  even  after  a  number 
of  severe  attacks. 

In  considering  the  morbid  anatomy  of  angina  it  was  emphasized  that  in 
the  majority  of  cases  the  condition  was  associated  with  arterio-sclerosis 
(aortic,  coronary  or  general)  and  some  form  of  organic  heart  disease, 
usually  chronic  myocarditis.  An  individual  suffering  from  cardio- 
vascular disease  may  either  be  free  from  symptoms  or  the  symptoms  may 
be  so  slight  as  to  pass  unnoticed,  and  yet  he  may  be  seized  with  an  attack 
of  angina  which  terminates  in  sudden  death.  Such  cases  are  usually 
due  to  thrombosis  or  an  embolus  of  one  of  the  coronary  arteries. 


ANGINA    PECTORIS  711 

In  another  and  larger  group,  the  initial  attack  may  occur  also  without 
premonitory  symptoms  but  the  patient  survives  only  to  succumb  in  a 
subsequent  seizure.  Such  individuals  may  suffer  from  a  number  of 
attacks  which  occur  at  irregular  intervals  and  may  extend  over  a  period 
of  years.  In  rare  instances  the  primary  paroxysm  is  followed  by  rapidly 
recurring  attacks  which  soon  prove  fatal. 

By  far  the  largest  number  of  victims  of  the  disease  manifest  some 
evidence  of  their  cardio-vascular  disease  prior  to  the  appearance  of  angina 
and  in  addition  they  are  apt  to  suffer  from  symptoms  which,  although  not 
typical  of  true  angina,  are  at  least  "anginoid"  in  character.  In  such 
cases  there  may  be  persistent  arrhythmia  and  an  ever-increasing  suscepti- 
bility to  attacks  of  dyspnea,  especially  after  exertion.  Still  more  sig- 
nificant is  a  feeling  of  tightness  across  the  upper  part  of  the  chest  or  a 
sense  of  pressure  beneath  the  sternum  after  exercise  or  a  full  meal.  These 
lesser  feelings  of  tightness  and  distress  in  the  chest  may  become  increas- 
ingly painful,  finally  developing  into  the  pain  characteristic  of  true  or 
major  angina. 

In  most  instances  the  anginal  attack  can  be  traced  to  a  definite 
exciting  cause.  The  most  frequent  source  is  muscular  exertion  such  as 
walking  briskly  or  running  upstairs.  Sudden  emotion,  especially  anger, 
is  not  infrequently  the  cause  of  a  seizure.  In  not  a  few  instances 
distention  of  the  stomach  following  a  full  meal  precipitates  an  attack 
and  accounts  for  some  of  the  cases  of  sudden  death  ascribed  to  acute 
indigestion. 

As  the  result  of  exertion  or  intense  mental  emotion,  there  develops 
suddenly  in  the  upper  chest  a  feeling  of  intense  pressure,  as  though  it 
were  held  in  a  vise,  or  there  is  pain  sometimes  agonizing  in  character,  which 
centers  in  the  substernal  region  and  radiates  to  the  left  shoulder  and 
down  the  left  arm  to  the  elbow  or  wrist.  The  pain  may  extend  down 
both  arms;  or  it  may  be  reflected  to  the  neck  and  jaw;  or  it  may  be  abdomi- 
nal. Rarely  it  is  felt  in  one  testicle.  Coincidently  with  the  pain  there 
is  great  mental  apprehension  and  a  fear  of  impending  death.  The 
patient,  if  he  has  been  walking,  stands  still  or  sits  down  at  once  and 
remains  breathless  and  immovable  until  the  attack  has  passed  off. 
As  a  rule,  the  seizure  lasts  from  a  few  seconds  to  a  minute  or  two. 
During  the  attack  there  is  usually  marked  pallor  or  an  ashy  gray  appear- 
ance of  the  face  and  there  may  be  also  profuse  sweating. 

Dyspnea,  while  not  an  essential  feature  of  angina  pectoris,  sometimes 
occurs  during  the  attack.  It  may  resemble  asthma,  the  breathing  being 
of  a  wheezy  character;  in  other  cases  acute  pulmonary  edema  and  the 
expectoration  of  thin  blood-tinged  fluid  may  occur.  When  respiratory 
phenomena  do  occur,  they  are  usually  coincidents. 

The  attack  may  terminate  in  several  ways:  (1)  It  may  be  cut  short 
by  sudden  death;  (2)  the  patient  may  pass  away  in  syncope;  (3)  he  maj' 
faint ;  (4)  the  attack  passes  off  leaving  the  patient  with  a  feeling  of  exhaustion 
lasting  for  a  day  or  so;  and  (5)  recovery  from  the  seizure  may  be  complete 
in  an  hour  or  less  time.  With  the  subsidence  of  the  attack  there  may  be 
eructations,  or  the  voiding  of  a  considerable   quantity  of  clear  urine. 

Occasionally  patients  with  cardio-vascular  disease  suffer  from  a  vas- 
cular crisis  in  which  there  are  pallor,  great  weakness,  and  a  fear  of  im- 
pending death,  but  no  pain.  Such  attacks  are  referred  to  as  angina 
sine  dolore. 


712  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

Physical  Signs. — There  is  nothing  distinctive  in  the  physical  findings 
during  the  height  of  the  seizure;  furthermore,  the  attack  is  usually  so 
ephemeral  and  the  symptoms  so  urgent  there  is  little  time  for  a  detailed 
examination.  There  is  very  frequently  arrhythmia  but  it  is  noteworthy 
that  in  many  instances  the  heart  action  is  slow  and  regular.  Xot  infre- 
quently the  radial  pulse  on  one  side  is  smaller  than  the  other. 

Examination  of  the  patient  during  the  intervals  usually  shows  that 
there  are  evidences  of  arterio-sclerosis  and  organic  disease  of  the  heart 
either  in  the  form  of  a  chronic  valvular  lesion  or  a  chronic  myocarditis 
or  both. 

Janeway  attaches  great  importance  to  the  presence  of  arterial  hyper- 
tension in  the  diagnosis  of  true  angina.  He  believes  that  in  the  absence 
of  any  demonstrable  anatomical  change  in  the  heart  the  occurrence  of  a 
blood-pressure  of  over  180  mm.  can  be  held  accountable  for  the  seizure. 
The  negative  evidence,  however,  is  not  so  convincing.  Especially  is  this 
true  in  very  severe  attacks  when  the  pressure  may  be  low.  During 
the  attack  the  blood-pressure  may  rise  or  it  may  fall.  With  intense 
pain  regularly  following  slight  exertion,  and  pallor  of  the  face  during  the 
attack,  a  low  blood-pressure  seems  to  augur  a  bad  outlook  (Janeway) . 

Diagnosis. — The  recognition  of  true  angina  pectoris  is  not  difficult 
if  due  consideration  is  given  to  the  symptoms  and  the  associated  cardio- 
vascular lesions.  Additional  aids  are  furnished  by  the  age,  the  sex  and 
the  occupation  of  the  individual. 

INCIPIENT  ANGINA  PECTORIS 

In  this  form  of  the  disease  a  sensation  of  substernal  soreness  or 
oppression  or  slight  pain  may  be  the  only  manifestation.  These  minor 
seizures  may  occur  for  a  time  and  then  cease  entirely;  or  they  may 
become  increasingly  severe  and  finally  have  all  the  features  of  angina 
major. 

Etiology. — The  etiological  factors  of  incipient  angina  are  essentially 
the  same  as  in  the  major  type  of  the  disease.  There  are  two  conditions, 
however,  which  deserve  special  mention  in  considering  these  anginoid 
or  milder  attacks  of  pain,  namely,  syphilitic  aortitis  and  arterial  hyperten- 
sion. And  while  we  have  already  referred  to  this  relationship,  the 
importance  of  this  group  of  cases  cannot  be  overemphasized. 

When  the  aorta  becomes  the  seat  of  syphilitic  disease,  it  is  the  first 
part  of  the  vessel  just  beyond  the  aortic  ring  that,  as  a  rule,  is  affected. 
The  aortic  valves  are  also  very  frequently  involved.  This  lesion  is  quite 
apt  to  produce  a  feeling  of  soreness  or  oppression  beneath  the  sternum 
or  there  may  be  distinct  pain.  Sometimes  these  symptoms  are  the 
precursors  of  true  angina  or  aneurism. 

Another  very  important  group  is  comprised  of  those  in  whom  a  feel- 
ing of  substernal  distress  or  tension  are  associated  with  slight  muscular 
exertion,  such  as  walking  briskly,  climbing  a  stair  or  the  indulging  in  any 
form  of  exertion  following  a  meal.  On  the  other  hand,  the  symptoms 
may  be  due  to  emotion  or  excitement.  Hypertension  should  always 
be  thought  of  under  these  circumstances  as  patients  with  an  abnormally 
high  blood-pressure  (200  to  250  mm.)  very  commonly  suffer  from  some 
substernal  distress  after  slight  exertion  or  as  the  result  of  excitement.  The 
hypertension  may  occur  without  there  being  any  demonstrable  lesion 


ANGINA    PECTORIS  713 

of  either  the  vessels  or  heart.  It  is  of  itself,  however,  sufficient  evidence 
that  organic  disease  will  sooner  or  later  manifest  itself.  Under  these 
circumstances  the  importance  of  the  anginoid  symptoms  cannot  be  over- 
estimated. 

Morbid  Anatomy. — The  pathology  of  incipient  angina  is  identical 
with  that  of  the  major  form. 

Symptoms. — The  lighter  attacks  of  angina,  in  the  beginning,  consist 
of  nothing  more  than  a  transient  sense  of  oppression  or  distress  beneath 
the  sternum  which  is  neither  sharply  localized  nor  does  it  radiate.  In 
some  cases  there  may  be  slight  pallor  and  faintness,  but  there  is  lacking 
the  shock  and  fear  of  impending  death  which  characterizes  the  major 
seizures.  These  mild  attacks  may  cease  entirely  or  they  may  recur 
for  years.  In  not  a  few  instances,  however,  the  feeling  of  tightness 
is  replaced  by  pain  which  gradually  becomes  worse,  and  more  and  more 
assumes  the  character  of  the  pain  encountered  in  true  angina. 

Physical  Signs. — Physical  examination  of  the  heart  and  peripheral 
arteries  may  be  entirely  negative.  But  in  many  cases  a  careful  exami- 
nation of  the  cardio-vascular  system  will  detect  some  change  which 
will  suggest  the  cause  of  the  heart  pain.  There  may  be  slight  cardiac 
hypertrophy;  or  the  presence  of  an  aortic  murmur,  either  systolic  or 
diastolic,  less  frequently  a  mitral  murmur;  or  there  may  be  some  thick- 
ening of  the  peripheral  arteries. 

In  every  case  presenting  anginoid  symptoms  a  Wassermann  test  and 
blood-pressure  estimation  should  be  made.  In  addition,  the  retinal 
vessels  should  be  inspected  as  they  not  infrequently  will  show  sclerotic 
changes  prior  to  their  detection  in  the  peripheral  arteries. 

Diagnosis. — While  it  is  probabh^  true  that  anginoid  symptoms  in 
some  instances  may  be  functional  in  origin,  it  is  equally  true  that  they  are 
often  indicative  of  serious  organic  trouble.  It  is  not  easy  always  to 
differentiate  between  the  two  types.  The  only  safe  rule  to  follow  is  to 
exclude  carefully  every  possible  organic  lesion.  Only  when  the  blood- 
pressure  is  normal,  the  Wassermann  test  negative,  and  there  is  no 
discoverable  cardiac  or  vascular  lesion,  is  one  justified  in  ascribing  to  the 
symptoms  a  functional  origin. 

ANGINA  PECTORIS  VASOMOTORIA 

(Pseudo-angina,  Mock,  Spurious  or  False  Angina) 

These  terms  are  applied  to  those  instances  of  precordial  pain  due  to 
vasomotor  disturbances.  Aside  from  the  occurrence  of  pain,  which,  as  a 
rule,  has  but  a  superficial  resemblance  to  true  angina,  attacks  of  this 
nature  have  nothing  in  common  with  true  angina  of  either  the  major  or 
incipient  type. 

Etiology. — Vasomotor  angina  may  occur  at  any  age  although  rare 
before  the  twentieth  year.  It  is  encountered  more  frequently  in  females 
than  males  and  is  of  relatively  frequent  occurrence  in  women  who  are 
emotional  or  neurotic.  In  common  with  other  manifestations  of  an 
unstable  nervous  system,  false  angina  may  show  itself  in  several  succes- 
sive generations.  During  the  menopause  vasomotor  disturbances  are 
common  and  not  a  few  women  during  this  period  suffer  from  false  angina. 

A  very  common  complaint  is  a  feeling  of  pain  or  oppression  just 
beneath  the  heart,  usually  associated  with  dyspeptic  symptoms,  espe- 


714  DISEASES    OF    THE    PERICARDIUM,    HEART,    AXD    AORTA 

cially  flatulency.  In  the  majority  of  cases  the  pain  is  due  to  false  and  not 
true  angina.  But  it  is  to  be  borne  in  mind  that  gastric  distention  fol- 
lowing a  meal  sometimes  provokes  an  attack  of  true  angina.  The  loca- 
tion and  character  of  the  pain  will  serve  to  distinguish  the  two  conditions 
in  most  cases. 

Precordial  pain  is  not  uncommon  in  those  addicted  to  the  excessive 
use  of  tea,  coffee  or  tobacco.  There  are  some  who  believe  that  nicotine 
poisoning  is  of  itself  a  cause  of  true  angina.  The  evidence  on  this  point, 
however,  is  not  convincing.  Many  of  those  who  are  subject  to  attacks  of 
true  angina  are  at  the  same  time  heavy  smokers.  It  seems  more  likely  that 
the  excessive  use  of  tobacco  merely  provokes  an  attack  in  an  individual 
with  a  latent  organic  lesion  rather  than  being  the  cause  of  the  lesion. 

Attacks  of  precordial  pain,  functional  in  origin,  may  follow  one  of  the 
acute  infectious  diseases,  notably  influenza. 

Morbid  Anatomy. — In  the  great  majority  of  the  cases  of  false  angina 
there  is  no  morbid  anatomy.  The  pain  may  be  ascribed  to  "a  disordered 
innervation  of  the  vessels,  peripheral  or  visceral,  resulting  in  their  con- 
traction, causing  an  increased  pressure  of  blood  in  the  cavities  of  the 
heart,  and  a  consequent  embarrassed  action  with  pain  and  dyspnea" 
(Powell).  Furthermore,  the  disturbance  of  the  vasomotor  mechanism 
may  manifest  itself  with  cold,  numb  and  blue  extremities,  or  attacks  of 
headache,  neuralgia,  etc. 

Symptoms. — Subjects  of  tins  form  of  angina  may  have  pain  which  is 
indistinguishable  from  that  occurring  in  the  organic  form  of  the  disease 
although  it  is  rarely  as  severe  nor  does  it,  as  a  rule,  radiate  to  the  left  arm. 
Furthermore,  the  pain  in  false  angina  may  be  diffuse  or  it  may  have  its 
point  of  greatest  intensity  beneath  the  heart  as  in  cases  of  indigestion. 
In  other  instances  the  pain  is  sharp  and  shooting  in  character.  This  type 
of  pain  is  not  infrequent  in  those  addicted  to  the  use  of  tea,  coffee,  or 
tobacco.  Instead  of  pain  there  may  be  a  sense  of  oppression  about  the 
heart.  Palpitation  of  the  heart  is  commonly  associated  with  the  pain 
and  may  be  the  most  annoying  feature  of  the  attack. 

One  of  the  striking  features  of  true  angina  is  the  immobility  of  the 
patient  during  a  seizure,  whereas  in  this  form  there  may  be  great  restless- 
ness, the  patient  moving  or  tossing  about  during  the  attack.  In  addition 
to  the  pain  and  palpitation  there  may  be  more  or  less  dyspnea  and  a  sense 
of  air  hunger  in  mock  angina,  in  marked  contrast  to  true  angina  in  which 
the  breath  is  held. 

Precordial  pain,  functional  in  type,  is  usually  sudden  in  onset  and  lasts 
but  a  brief  time ;  a  sense  of  oppression  or  dull  pain  may  persist,  however, 
for  a  half  hour  or  longer.     In  very  severe  cases  the  patient  may  faint. 

Usually  the  attacks  occur  at  irregular  intervals  and  are  apt  to  follow 
overexcitement,  excessive  smoking  or  an  attack  of  indigestion;  in  hysteri- 
cal individuals  there  may  be  a  number  in  one  day.  The  occurrence  of 
precordial  pain  is  very  apt  to  make  the  patient  apprehensive  that  serious 
cardiac  disease  is  present  and  this  of  itself  tends  to  induce  an  attack. 
This  form  of  angina  is  never  fatal. 

In  considering  the  etiology  of  the  affection  it  was  pointed  out  that 
emotional  or  neurotic  women  were  most  subject  to  false  angina;  and  that 
other  evidences  of  vasomotor  disturbance  were  common.  Among  the 
latter  may  be  mentioned  coldness  and  numbness  of  the  extremities,  at- 
tacks of  migraine,  neuralgia  and  flushes  of  heat.     The  patient  is  usually 


AXGIXA    PECTORIS  715 

of  spare  build  although  plethoric  women  at  the  menopause  are  very  sus- 
ceptible to  attacks  of  precordial  pain. 

Physical  Signs. — Examination  of  patients  subject  to  angina  vaso- 
motoria may  elicit  nothing  abnormal  in  the  heart;  neither  is  there  disease 
of  the  arteries.  On  the  other  hand  the  heart  action  may  be  very  rapid 
and  irregular.  During  an  attack  the  pulse  is  often  small  and  irregular 
or  intermittent. 

Diagnosis. — The  distinction  between  this  type  of  precordial  pain  and 
true  angina  rests  largely  on  the  presence  or  absence  of  organic  disease  of 
the  heart  and  blood-vessels.  Furthermore,  false  angina  is  more  common 
in  neurotic  women;  it  is  encountered  at  an  earlier  age  period;  and  the 
attack  lacks,  as  a  rule,  most  of  the  characteristic  features  of  true  angina. 

Allbutt1  has  given  a  very  clear  description  of  mock  or  spurious  angina. 
It  is  notable,  he  states,  how  obviously  the  heart  is  upset — palpitation, 
arrhythmias,  sudden  stoppages  and  accelerations,  which  are  not  charac- 
ters of  true  angina.  The  so-called  "heart  pain"  present  in  many,  if  not  all, 
of  these  cases,  the  sense  of  distention  of  the  whole  upper  chest,  often  with 
submammary  pain  and  local  hyperesthesia,  are  neither  in  seat  nor  in  kind 
like  the  pain  of  angina..  In  addition  the  breathing,  far  from  being  held 
as  in  angina,  is  panting;  the  bodily  state  is  not  awe-stricken  but  restless 
and  agitated. 

1  ''Diseases  of  the  Arteries,  Including  Angina  Pectoris,"  vol.  ii,  1915. 


CHAPTER  XXX 
DISEASES  OF  THE  AORTA 

ACUTE  AORTITIS 

Etiology. — Acute  inflammatory  changes  involving  a  portion  or  all  of 
the  aorta  are  undoubtedly  of  more  frequent  occurrence  than  is  usually 
believed  to  be  the  case.  Very  often  the  lesion  first  reveals  itself  at  the 
autopsy  but  in  not  an  inconsiderable  number  the  condition,  during  life, 
is  either  entirely  overlooked  or  its  presence  is  masked  by  preexisting 
symptoms  and  physical  signs.  The  most  complete  description  of  acute 
aortitis  is  given  by  Allbutt.1 

Acute  aortitis  may  occur  as  a  complication  or  sequel  of  one  of  the 
acute  infectious  diseases,  such  as  scarlet  fever,  smallpox,  erysipelas, 
septicemia,  influenza  or  typhoid  fever.  The  importance  of  typhoid 
fever  as  an  exciting  cause  of  acute  endarteritis  has  been  emphasized 
by  French  observers  and  in  this  country  by  Thayer.  In  52  cases  of 
typhoid  fever  the  aorta  showed  evidences  of  a  recent  endarteritis 
in  21  instances  (Thayer).  Broadbent  states  that  in  young  children 
who  have  died  of  pneumonia,  septicemia  or  some  acute  bacterial  infection, 
he  has  frequently  seen  at  the  autopsy  small,  yellow  and  elevated  patches 
in  the  aorta  which  he  regarded  as  instances  of  acute  degeneration  resulting 
from  the  action  of  microorganisms  or  their  toxins.  According  to  Allbutt 
acute  aortitis  is  not  of  infrequent  occurrence  in  children  suffering  from 
acute  rheumatic  fever. 

When  it  develops  during  the  course  of  one  of  the  acute  infections, 
acute  aortitis  seems  to  be  less  severe  and  less  apt  to  cause  serious  symptoms 
than  when  superimposed  on  a  chronic  aortitis.  Some  observers  believe, 
at  least  in  so  far  as  clinical  evidence  is  concerned,  that  in  the  great  major- 
ity of  cases  the  acute  lesion  develops  only  when  the  vessel  has  become  the 
site  of  a  chronic  lesion.  This  is  particularly  true  in  gouty  individuals 
whose  vessels  have  become  atheromatous.  It  may  occur  also  in  cases  of 
chronic  lead  poisoning. 

Since  the  discovery  of  the  spirocheta  pallida  and  the  Wassermann 
reaction  it  has  become  clear  that  many  cases  which  would  formerly  have 
been  considered  as  simple  acute  aortitis  are  in  reality  instances  of 
syphilitic  aortitis. 

Morbid  Anatomy. — Acute  aortitis  is  apt  to  arise  during  the  course 
of  any  of  the  acute  infections  and  pass  away  unnoticed.  With  the  ex- 
ception of  syphilis  the  acutely  inflamed  aorta  may  show  no  changes  to 
the  naked  eye  or  the  changes  may  be  so  slight  as  to  pass  unnoticed  unless 
carefully  looked  for.  Appropriate  staining  methods  will  usually  bring- 
out  very  clearly  the  acute  degenerative  areas  (Fig.  395).  Occasionally 
the  intima  may  be  reddened  or  it  may  have  lost  its  glistening,  polished 
appearance  as  the  result  of  a  thin  fibrinous  exudate  over  the  surface.     The 

^'Diseases  of  the  Arteries,  Including  Angina  Pectoris, ""  vol.  ii,  1915. 

716 


Fig.  395. — 'Acute  aortitis.  From  a  woman  aged  twenty-eight.  Septicemia  follow- 
ing abortion.  Specimen  stained  concurrently  with  Sudan  III  and  Scharlach  R.  Acute 
fatty  degenerative  areas  deeply  stained.  Normal  aorta  should  exhibit  no  more  stain 
than  shown  in  palest  areas.      (Jefferson  Medical  College  Museum.) 


DISEASES    OF    THE    AORTA  717 

first  part  of  the  aorta  may  be  dilated  and  in  most  instances  a  recession 
to  the  normal  usually  takes  place. 

As  usually  seen,  the  degenerative  changes  are  characterized  by  the 
presence  of  plaques  ranging  in  size  from  that  of  a  pinhead  to  a  circle 
an  inch  in  diameter.  Not  infrequently  the  plaques  have  coalesced. 
Their  appearance  varies  with  the  stage  of  the  process.  At  first  they  are 
slightly  elevated,  soft,  pinkish-white  or  gray  in  color  and  opalescent ; 
later  they  become  firmer  and  yellowish  in  color.  Microscopically  the 
patches  are  seen  to  consist  of  an  infiltration  of  the  subendothelial  tissue 
with  round  cells,  spindle  cells  and  stellate  cells  arranged  in  layers. 

As  the  first  part  of  the  aorta  bears  the  brunt  of  the  infection,  the 
orifices  of  the  coronary  arteries  are  sometimes  partially,  or  entirely, 
occluded  as  the  result  of  swelling  of  the  adjacent  tissues.  It  is  this 
closure  of  the  coronary  vessels  that  gives  rise  to  the  anginoid  pain. 

Occasionally  ulcerative  endocarditis  may  extend  and  involve  the 
root  of  the  aorta.  Rarely  in  cases  of  septicemia,  abscesses  may  form  be- 
tween the  external  and  middle  coats  of  the  artery  and  rupture  inward. 

Inasmuch  as  the  vessel  is  often  chronically  diseased  there  may  be 
noted  also  all  grades  of  atheromatous  degeneration. 

Symptoms. — An  individual  suffering  with  an  acute  inflammation  of 
the  root  of  the  aorta  may  be  subject  to  attacks  of  difficulty  in  breathing 
and  a  sense  of  oppression  in  the  chest.  Pain  is  an  important  diagnostic 
symptom.  Allbutt1  describes  the  pain  as  having  its  "origin  under  the 
sternum,  often  at  the  junction  of  the  first  and  second  thirds  of  the  bone, 
and  a  sense  of  constriction  or  compression,  as  if  the  chest  were  in  a  vise 
or  the  breast  bone  crushed  inward  by  an  iron  bar.  And  this  pain  may 
come  in  any  degree,  from  a  transient  sense  of  tightness  or  oppression  about 
the  upper  sternum  to  utter  torture."  Sansom  describes  it  as  being 
"of  a  burning  or  tearing  character,  with  a  sensation  of  constriction 
or  tension  referred  to  the  sternum."  In  most  cases  there  is  a  tendency 
for  the  pain  to  radiate  from  the  midsternal  region  into  the  left  arm; 
occasionally  into  both  arms,  but  rarely  into  the  right  alone.  Among 
the  symptoms  of  lesser  importance  are:  fatigue,  insomnia,  vertigo, 
flatulence,  nausea  and  sometimes  vomiting.  Fever  is  often  present. 
The  paroxysmal  dyspnea  and  the  substernal  pain  are  the  important 
features  of  acute  aortitis. 

Physical  Signs. — Allbutt  lays  great  stress  on  the  physical  signs, 
especially  the  percussion  findings  and  the  character  of  the  aortic  second 
sound. 

Inspection. — There  may  be  undue  throbbing  of  the  carotid  arteries 
and  in  some  cases  Potain's  sign  may  be  noted.  This  sign  consists  of 
an  abnormal  upward  displacement  of  the  subclavian  arteries  so  that 
they  are  seen  or  felt  to  beat  in  the  hollow  above  the  clavicles.  This  is 
due  to  dilatation  of  the  aorta,  causing  its  branches  to  be  lifted  to  a  higher 
plane.  In  the  normal  state  the  subclavian  artery  does  not  rise  above  the 
clavicle. 

Percussion. — The  area  of  dulness  will  be  found  to  occupy  the  manu- 
brium, or  at  first  the  middle  third  of  it,  with  an  adjacent  area  of  the  second 
rib  and  third  interspace  one  or  two  finger' s-breadth  to  the  right.  The 
dulness  about  mid-manubrium  is  generally  quite  decisive.     It  may  cross 

1  "Diseases  of  the  Arteries,  Including  Angina  Pectoris,"  vol.  ii.  1915. 


718  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

over  a  little  to  the  left  but  is  never  so  marked  as  on  the  right.  Dulness 
may  be  elicited  also  posteriorly  over  the  third  and  fourth  dorsal  vertebrae. 

Auscultation.- — Allbutt  places  great  reliance  on  the  quality  of  the  aortic 
second  sound  but  finds  it  difficult  to  describe.  The  term  ''clanging" 
he  objects  to.  The  quality  of  the  sound  is  more  tympanitic.  Potain 
has  termed  it  the  bruit  de  tabourka  from  its  resemblance  to  the  sound 
produced  by  an  Algerian  drum,  which  is  made  of  an  earthen  pot  with  a 
skin  stretched  over  it.  In  some  cases  there  may  be  heard  at  the  base 
of  the  heart  a  pericardial  friction  rub. 

The  aortic  ring  may  become  dilated  or  the  valves  may  become 
inflamed  as  the  result  of  extension  from  the  aorta.  If  this  occurs,  a 
systolic  or  a  diastolic  murmur  or  both  may  be  heard. 

Diagnosis. — Acute  aortitis  may  be  confused  with  any  of  the  conditions 
in  which  precordial  pain  is  the  dominant  symptom. 

Angina  pectoris  is  apt  to  cause  the  most  difficulty.  In  true  angina 
the  patient  is  usually  a  male,  in  good  circumstances  and  beyond  the  middle 
period  of  life.  There  is  also  an  associated  cardiac  lesion  and  evidences  of 
arterio-sclerosis.  Acute  aortitis,  on  the  other  hand,  may  occur  at  any  age 
period;  the  sexes  are  equally  liable;  and  it  also  may  occur  in  those  of  any 
walk  of  life.  The  pain  in  acute  aortitis  is  usually  localized  behind  the 
upper  part  of  the  sternum. 

Syphilitic  aortitis  is  characterized  by  symptoms  similar  to  the  acute 
inflammatory  form  of  aortitis.  The  presence  or  absence  of  the  Wasser- 
mann  reaction  would  be  the  deciding  factor. 

SYPHILITIC  AORTITIS 

Etiology. — The  discovery  of  the  spirocheta  pallida  and  the  Wasser- 
mann  reaction  have  made  it  clear  that  mesaortitis  is  often  of  syphilitic  ori- 
gin. Not  only  do  a  very  high  percentage  of  cases  having  lesions  involving 
the  aortic  valves  and  root  of  the  aorta  show  a  positive  Wassermann  reac- 
tion, but  in  addition  the  spirochetal  can  be  demonstrated  in  the  wall  of  the 
aorta.  The  susceptibility  of  the  first  part  of  the  aorta  to  syphilitic  in- 
fection has  long  been  known  although  the  definite  proof  is  of  comparatively 
recent  origin.  Larkin  and  Levy1  found  histological  evidence  of  syphil- 
itic aortitis  in  17  of  19  cases  giving  a  positive  Wassermann  reaction.  In 
a  series  of  47  cases  of  aortic  insufficiency  Longcope2  obtained  a  positive 
Wassermann  reaction  in  35,  or  74.4  per  cent.  These  results  were  further 
confirmed  by  finding  in  7  cases  at  autopsy  lesions  typical  of  syphilitic 
mesaortitis  and  by  the  discovery  in  3  cases  of  spirochetal  in  the  wall  of 
the  aorta.  In  a  more  recent  article  Longcope3  expresses  the  belief  that  not 
less  than  three-fourths  of  all  cases  of  aortic  insufficiency  are  syphilitic  in 
origin.  Syphilitic  aortitis  also  furnishes  the  explanation  of  the  frequency 
of  aneurisms  of  the  arch  of  the  aorta. 

The  result  of  these  comparatively  recent  additions  to  our  knowledge  of 
disease  of  the  aortic  valves  and  root  of  the  aorta  has  been  to  establish  a 
distinct  group  in  which  the  etiology  and  pathology  are  essentially  different 
from  other  lesions  which  present  much  the  same  symptoms  and  physical 
signs. 

1  New  York  State  Jour.  Med.,  December,  1915. 

2  Report  of  Ayer  Clinical  Laboratory,  Pennsylvania  Hospital,  1910,  No.  6. 

3  Arch.  Int.  Med.,  January,  1913. 


DISEASES    OF    THE    AORTA  719 

Syphilitic  aortitis  is  encountered  most  frequently  among  those  of  early 
middle  life.  As  in  the  case  of  other  syphilitic  manifestations,  the  con- 
dition occurs  more  often  in  males  than  in  females.  Among  negroes  aortic 
insufficiency  is  very  frequently  syphilitic  in  origin.  The  condition  may  be 
encountered  also  in  congenital  syphilis.  Rebaudi1  in  a  study  of  the  aortas 
of  new-born  children  with  spirochete  in  the  principal  organs  found  13  of 
them  abnormal.  The  lesions  were  similar  to  those  of  the  aortitis  of  ac- 
quired syphilis  in  adults. 

Morbid  Anatomy . — The  initial  change  consists  of  a  small-celled  in- 
filtration of  the  media  accompanied  by  an  atrophy  of  both  the  muscular 
and  elastic  layers.  The  intima  is  not  primarily  involved  but  later  under- 
goes proliferative  thickening  (Adami  and  Nichols).  Eventually  the 
fibrosis  gives  place  to  atheromatous  changes. 

Syphilitic  aortitis  is  always  confined  to  and  often  sharply  localized  in 
the  arch  of  the  aorta.  In  some  instances  it  involves  only  the  first  part  of 
the  root  of  the  aorta.  The  gross  appearance  is  described  by  Longcope  as 
follows:  The  margin  of  the  sclerotic  area  is  very  abrupt,  while  the  aorta 
beyond  the  lesion  is  quite  smooth.  In  the  most  extensive  areas  are 
patches  of  thickening  from  2  to  3  cm.  in  diameter.  The  central  portion 
of  these  patches  is  elevated,  gray  and  somewhat  succulent  in  appearance, 
while  the  margins  are  yellowish  and  crinkled.  The  sclerosis,  when  marked, 
is  characterized  by  an  irregular,  corrugated  or  crinkled  thickening  of  the 
aortic  wall,  showing  small  pits  and  sometimes  minute  aneurismal  dilata- 
tions. Often  the  bases  of  these  small  aneurisms  are  so  thin  that  they 
transmit  light.  While  calcification  does  occur  the  usual  appearance  is 
rather  a  rubbery,  pliable  thickening  (Fig.  396).  The  aortic  valves  also 
show  the  same  rubbery  thickening  when  extensively  involved  and  occasion- 
ally there  are  crescentic  lines  of  whitish-yellow  thickening. 

The  foregoing  picture  is  essentially  different  from  that  encountered 
in  rheumatic  endocarditis  in  which  the  aorta  is  smooth  and  delicate  in 
appearance.  It  also  differs  from  the  lesions  encountered  in  general 
arterio-sclerosis.  In  the  latter  condition  the  atheromatous  changes  are 
not  confined  to  the  root  of  the  aorta  but  involve  the  entire  vessel  and  are 
often  more  marked  in  the  thoracic  and 'especially  the  abdominal  aorta. 

Symptoms. — In  the  majority  of  cases  of  syphilitic  aortitis  both  the 
symptoms  and  physical  signs  are  those  of  aortitic  insufficiency.  The 
importance  of  this  fact  cannot  be  overestimated.  If  the  lesion  is  syphi- 
litic in  origin  specific  treatment  will  arrest  its  progress  and  if,  as  not  infre- 
quently happens,  the  disease  is  confined  to  the  supra-aortic  area  the  valves 
may  be  saved  from  damage. 

"There  will  be  fewer  oversights  in  particular  cases  during  life  if  the 
suspicion  that  an  aortic  lesion  may  be  syphilitic  is  always  with  us.  Even 
if  we  can  elicit  no  evidence  of  an  infection,  the  references  from  the  story 
of  the  case,  or  from  associated  changes  and  relics  elsewhere  on  the  body, 
will  generally  bring  us  to  a  moral  certainty.  We  know  that  a  compara- 
tively young  man  of  otherwise  healthy  habits  does  not  suffer  from  local 
disease  of  the  aortic  region  of  the  heart  unless  it  be  in  consequence  of 
some  extraordinary  muscular  stress,  or  of  rheumatic  fever,  or  of  syphilis; 
if  then  such  muscular  stress  and  rheumatism  be  dismissed,  we  fall  back 
upon  syphilis,  as  we  do  with  a  like  assurance  in  the  case  of  aortic  aneurism 
in  such  a  person"  (Allbutt). 

1  Monatsch.  f.  Geburlsh.  u.  Gyn.,  June,  1912. 


720  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

In  a  smaller  percentage  of  cases  syphilitic  aortitis  occurs  in  an  acute 
form  with  substernal  pain,  a  sense  of  constriction  in  the  chest,  dyspnea 
and  at  times  angina  like  attacks  of  pain.  According  to  Blumer1  the  facies 
in  the  syphilitic  patients  is  often  quite  different  from  that  seen  in  the 
other  forms  of  aortic  insufficiency.     Instead  of  the  vivid  coloring  of 


Fig.  396. — Syphilitic  aortitis.  In  this  specimen  the  syphilitic  process  has  extended 
downward  along  the  aortic  wall  and  involved  the  coronary  orifices  and  the  aortic  leaflets. 
The  smooth,  more  or  less  sharply  circumscribed  rubbery  appearance  of  the  lesions  is  shown. 
Also  the  absence  of  calcification. 

rheumatic  aortic  disease,  there  is  often  pallor,  with  a  yellow  tinge  ap- 
proaching the  subicteric.  Psychic  manifestations  are  also  more  frequent 
in  the  syphilitic  type.  In  cases  of  this  type  a  murmur  is  usually  absent 
but  a  gradual  weakening  of  the  first  sound,  indicative  of  slight  valvular 
involvement,  may  be  noted.     Grau2  states  that  in  the  syphilitic  cases  the 

1  Albany  Med.  Annals,  August,  1914. 
2Zeit.f.  Klin.  Med.,  1911,  lxxii. 


DISEASES    OF    THE    AORTA  721 

arterial  phenomena  are  less  marked  than  in  the  rheumatic  cases.  This  is 
due  to  the  fact  that  the  entire  aorta  is  often  dilated  and  has  lost  its  elastic- 
it}' — hence  the  violent  recoil  of  the  blood  current  is  modified. 

In  23  cases  studied  by  Grau  the  interval  between  the  infection  and 
the  manifestation  or  aortitis  was  from  six  to  forty-one  years.  Blumer 
believes  that  the  period  which  elapses  between  the  primary  infection 
and  the  appearance  of  symptoms  of  aortitis  averages  eighteen  years. 

Whether  the  aortic  insufficiency  or  the  acute  type  of  aortitis  is  syphi- 
litic in  origin  will  rest  on  the  presence  of  a  positive  Wassermann  reaction. 
In  cases  in  which  the  aortic  lesion  occurs  in  combination  with  damage 
to  the  mitral  and  tricuspid  valves,  a  rheumatic  origin  of  the  trouble  is 
more  than  probable,  but  in  isolated  aortic  lesions  it  is  becoming  more 
and  more  apparent  that  syphilis  is  the  chief  offender. 

Physical  Signs. — The  physical  findings  are,  in  most  cases,  those 
encountered  in  aortic  insufficiency.  When  the  disease  is  confined  to 
the  supra-aortic  area  the  physical  signs  are  those  of  acute  or  chronic 
aortitis. 

Diagnosis. — The  early  symptoms  and  signs  of  syphilitic  aortitis 
are  as  follows:  Dyspnea,  which  is  often  paroxysmal  in  character;  pain, 
or  a  feeling  of  oppression  in  the  precordium,  in  some  instances  the  pain 
is  felt  under  the  short  ribs,  in  others  the  pain  is  due  to  angina  pectoris. 
More  or  less  cardiac  hypertrophy  is  present  and  the  vessels  of  the  neck 
show  increased  pulsation.  Of  the  greatest  importance  is  the  presence 
of  a  positive  Wassermann  reaction  and  the  signs  of  or  the  demonstration 
by  the  X-rays  of  dilatation  of  the  aorta. 

CHRONIC  AORTITIS 
(Arterio-sclerosis  or  Atheroma  of  the  Aorta) 

Etiology. — Arterio-sclerosis  may  be  defined  as  a  local  or  general 
thickening  of  the  walls  of  the  arterial  tree  together  with  a  loss  of  elasticity 
due  to  an  overgrowth  of  fibrous  tissue  and  ultimately  to  the  develop- 
ment of  areas  of  degeneration  (atheroma). 

I.  A  general  thickening  and  hardening  of  the  arteries  is  an  almost 
constant  finding  in  people  of  advanced  years.  In  the  absence  of  any 
predisposing  cause,  the  change  begins  to  show  itself,  as  a  rule,  at  about 
the  middle  period  of  life  and  as  time  passes  the  sclerotic  process  tends  to 
increase.  While  the  entire  arterial  tree  shows  some  evidence  of  fibrosis 
the  change  is  not  usually  uniform.  In  one  individual  it  is  the  arch  of 
the  aorta  that  shows  the  most  advanced  lesions;  in  another  the  abdominal 
aorta  is  most  diseased;  while  in  still  another  it  is  the  cerebral  arteries 
that  have  suffered  most. 

The  frequency  with  which  different  parts  of  the  arterial  tree 
are  most  affected  are:  ascending  aorta,  the  arch,  descending  aorta, 
abdominal  aorta,  iliacs,  crurals,  coronary  arteries  and  cerebral  arteries 
( Rokitansky). 

II.  In  some  individuals  there  is  apparently  an  inherited  predisposition 
to  early  arterial  degeneration.  The  process  occurs  relatively  early  in 
life  and  frequently  brings  about  a  fatal  termination  at  an  age  when  the 
process  should  be  in  its  incipiency.  I  recall  one  family  in  which  both 
parents  died  as  the  result  of  arterio-sclerosis  and  three  of  the  children 
succumbed  to  the  same  disease  before  attaining  their  fiftieth  year. 

46 


722  DISEASES    OF    THE    PERICARDIUM,    HEART,    AXD    AORTA 

III.  The  male  sex  shows  a  higher  percentage  of  cases  than  the 
female  in  the  earlier  years  but  subsequent  to  the  menopause  females 
are  equally  liable. 

IV.  The  habits  of  the  individual  exercise  a  very  potent  influence  on 
aggravating  the  condition.  Among  those  in  comfortable  circumstances 
serious  arterial- changes  are  frequently  encountered,  especially  if  they 
have  "lived  high."  The  combination  of  overindulgence  at  the  table, 
the  immoderate  use  of  alcohol  and  lack  of  healthful  exercise  are  frequent 
causes  of  hastening  the  process.  There  are  many  cases  in  which  over- 
eating is  the  only  factor  (Osier). 

V.  Occupation  plays  a  very  important  role  in  bringing  about  arterio- 
sclerosis. In  one  class  of  patients  the  work  is  entirely  mental  and  at- 
tended with  a  constant  strain  on  the  nervous  system.  Thus  the 
banker  or  business  man  in  the  fifth  decade  who  is  constantly  engaged  in 
ventures  entailing  great  responsibility  and  long  hours  of  work  is  suddenly 
stricken  in  his  prime  with  a  fatal  apoplexy  or  his  health  is  permanently 
impaired  as  the  result  of  a  degenerated  heart  muscle.  An  even  more 
frequent  result  is  a  gradual  failure  of  health  as  the  result  of  associated 
changes  in  the  kidney.  The  occurrence  of  advanced  arterial  changes  in 
men  of  this  class  must  be  ascribed  to  their  high-pressure  methods  of 
■living  as  they  are  frequently  abstemious  in  their  habits  and  have  suffered 
from  neither  syphilis  nor  gout. 

The  other  extreme  is  the  common  laboring  man  who  for  years  has 
followed  a  laborious  occupation;  has  lived  in  insanitary  places;  has 
had  a  poor  dietary;  and  has  overindulged  in  alcohol.  The  most  extreme 
cases  of  arterio-sclerosis  I  have  encountered  have  been  in  individuals 
of  this  class.  Many  of  them  after  the  age  of  60,  possess  arteries  which 
certainly  deserve  the  name   "pipe-stem." 

VI.  Sooner  or  later  in  every  case  of  arterio-sclerosis  a  constant  accom- 
paniment is  a  diseased  kidney.  It  is  not  at  all  clear  which  is  the  ante- 
cedent trouble.  Some  observers  consider  that  the  cardio-vascular  changes 
result  from  defective  elimination:  others,  that  the  kidney  becomes 
affected  as  a  result  of  the  arterial  changes.  In  some  cases,  evidences  of 
nephritis  are  first  to  appear;  in  others  the  kidney  changes  manifest 
themselves  secondarily. 

VII.  Among  the  toxic  causes  lead  and  alcohol  are  the  most  important. 
Although  Cabot  discredits  the  influence  of  alcohol  as  a  predisposing  cause 
of  arterio-sclerosis  the  prevailing  opinion  is,  that  either  alone  or  in  asso- 
ciation with  other  factors,  it  cannot  be  disregarded. 

VIII.  Among  the  diseases  which  seem  especially  to  predispose  to 
arterial  changes  may  be  mentioned  syphilis,  gout,  rheumatism,  chronic 
arthritis  and  certain  of  the  acute  infections,  notably  typhoid  fever. 

Of  more  importance,  probably,  than  any  of  the  single  etiological 
factors  mentioned  is  syphilis.  In  so  far  as  the  aorta  is  concerned  it  is 
the  most  important  factor  as  syphilitic  arterio-sclerosis  frequently  takes 
the  form  of  a  mesaortitis.  As  a  race,  the  negro  is  especially  prone  to  de- 
velop marked  degenerative  changes  in  the  arteries  as  the  result  of  a 
luetic  infection.  Syphilitic  arteritis  has  been  found  to  be  a  very  common 
finding  among  the  West  Indian  negroes  employed  in  the  construction 
of  the  Panama  Canal,  while  in  this  country  the  occurrence  of  aortic 
aneurism    and    aortic  insufficiency  among  negroes  is  frequently  noted. 

Morbid  Anatomy. — In  considering  the    etiology  of  arterio-sclerosis 


DISEASES    OF    THE    AORTA  723 

it  was  shown  that  alterations  in  the  arteries  might  be  brought  about  by 
a  number  of  factors,  and  that  by  far  the  most  frequent  cause  was  a  physio- 
logical deterioration  incident  to  old  age. 

One  of  the  penalities  of  advancing  years  is  a  gradual  loss  of  elasticity 
of  the  arteries.  This  occurs  in  all  walks  of  life  irrespective  of  whether  the 
individual  has  or  has  not  been  subject  to  some  known  exciting  cause. 
In  some,  the  change  occurs  earlier  and  becomes  more  marked  than  in 
others,  possibly  as  the  result  of  a  hereditary  predisposition;  in  others, 
the  arterial  changes  are  hastened  as  the  result  of  disease,  such  as  syphilis, 
gout,  or  typhoid  fever;  in  still  others,  the  degenerative  change  is  delayed 
and  never  assumes  serious  proportions.  In  a  histological  study  of  the 
aorta  Klotz  has  shown  that  beginning  with  about  the  thirty-fifth  year, 
there  are  evidences  of  early  changes  in  the  vessel.  The  earliest  mani- 
festations consist  of  degenerative  changes  in  the  media;  with  advancing 
years  these  changes  become  more  and  more  marked  and  as  a  result  the 
vessel  gradually  loses  its  elasticity.  That  such  a  result  should  occur 
is  not  surprising  when  we  recall  the  physiology  of  the  circulation.  With 
each  systole  of  the  left  ventricle  the  aorta,  already  filled  with  blood,  has 
forced  into  it  a  fresh  supply.  To  accommodate  this  the  vessel  becomes 
slightly  distended  and  then  immediately  contracts.  In  addition  as  the 
blood  meets  with  resistance  in  the  peripheral  capillaries  there  is  a  recoil 
and  as  the  blood  is  prevented  from  escaping  backward  by  the  closure 
of  the  semilunar  valves,  the  aorta  is  again  subjected  to  a  strain.  Still 
another  factor  to  be  considered  is  that  the  pressure  is  always  increased 
by  curvature  or  tortuosity  of  the  blood-vessel.  If  then  we  consider 
that  from  70  to  80  times  each  minute,  every  hour  and  every  day  the 
aorta  is  subjected  to  repeated  dilatations  and  contractions  it  becomes 
apparent  that  there  will  come  a  time  when  the  elasticity  of  the  vessel 
loses  its  tone. 

The  type  of  arterio-sclerosis  occurring  in  relatively  young  men,  and 
which  is  brought  about  by  an  abnormally  high  blood-pressure  resulting 
from  working  and  living  at  high  pressure,  is  analogous  to  the  senile  form  in 
the  method  of  its  causation.  One  is  a  natural  result;  the  other  is,  so  to 
speak,  artificially  produced. 

The  gross  appearance  of  the  aorta  when  it  has  undergone  senile 
atheromatous  change  is  as  follows :  In  the  earlier  stage  the  ascending  por- 
tion and  the  arch  are  studded  with  round  or  oval,  slightly  elevated  patches 
of  a  yellowish  or  yellowish-white  color.  These  patches  vary  in  size  and 
number  and  in  the  thoracic  aorta  are  especially  marked  at  the  orifices  of 
the  branches  (see  Fig.  181). 

In  the  advanced  stage  of  the  disease  the  formation  intima  may  be  al- 
most entirely  obliterated  by  the  formation  of  rough,  calcareous  plaques 
(see  Fig.  398) ;  in  extreme  cases  the  aorta  may  be  reduced  to  a  rigid,  brittle 
tube  (see  Fig.  397).  Occasionally  a  chip  is  whipped  off  one  of  the  rough 
edges  of  a  calcareous  plaque  and  a  small  branch  of  one  of  the  distal  arter- 
ies is  occluded.  Gangrene  of  the  foot  and  leg  sometimes  is  produced  in 
this  way.  In  spite  of  the  rough  surface,  thrombi  are  formed  very  rarely. 
Another  unusual  sequel  is  ulceration  of  one  of  the  atheromatous  patches. 

Dilatation  of  the  vessel  may  be  present  varying  from  that  which  is  very 
slight  to  that  which  constitutes  a  true  aneurism. 

Although  the  gross  appearance  of  the  aorta  indicates  that  the  intima 
is  markedly  diseased  this  is,  in  reality,  a  secondary  manifestation.     The 


724  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

primary  change  occurs  in  the  media.  Klotz  has  shown  that  the  earliest 
change  is  to  be  noted  in  the  muscle  cells  of  the  media  which  first  undergo  a 
fatty  degeneration  and  later  a  powdering  with  fine  calcareous  granules. 
Eventually,  these  muscle  cells  become  shrunken  and  indistinguishable 
as  such.  Finally,  the  elastic  fibers  show  degenerative  change.  Following 
the  changes  in  the  media  the  subendothelial  layer  of  the  intima  becomes 
affected  and  the  slightly  elevated  patches  noted  in  the  early  stages  of  the 
disease  then  appear. 


Fig.  397. — Calcification  of  the  aorta.  The  entire  aorta  is  one  hard,  brittle,  rough, 
thickened,  calcareous  mass,  which  fractures  with  an  audible  snap  when  the  vessel  is  flexed. 
The  aortic  valves  share  in  this  process  of  calcification.  The  wall  of  the  left  ventricle  is 
greatly  thickened.  The  pericardium  is  thickened  and  the  subpericardial  fat  increased  in 
amount.      {Specimen  from  the  German  Hospital,  Philadelphia.) 

The  evolution  of  the  atheromatous  process  when  produced  by  the 
toxins  of  disease  or  specific  poisons,  such  as  lead,  are  essentially  the  same, 
namely,  a  primary  change  in  the  media  followed  sooner  or  later  by  degen- 
erative changes  in  the  intima. 

The  entire  subject  of  aortic  sclerosis  is  briefly  described  by  Adami  and 
Nicholls  as  follows:  (1)  In  the  vast  majority  of  cases,  if  not  in  all,  a  weak- 
ness and  giving  away  of  the  media  is  the  primary  anatomical  lesion. 

(2)  There  is  a  possibility  that,  as  the  result  of  a  subacute  proliferative 


DISEASES    OF    THE    AORTA 


725 


Fig.  398.-  -Calcification  of  the  aorta.  Specimen  showing  the  left  ventricular  cavity. 
The  aortic  valves  arc  thickened,  slightly  retracted,  and  contain  calcareous  deposits.  The 
aorta  is  greatly  thickened  and  its  entire  surface  is  covered  with  white  and  dark  yellow, 
roughened  and  projecting  calcareous  plates.  (Yellow  being  a  relatively  non-actinic  color, 
these  plates  appear  as  black  and  brown  in  the  reproduction.)  The  mitral  valve  is  moder- 
ately thickened.       ( S/tt-cinicii  from  /In   I'hiliult  Iphla  Hospital.) 


726  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

intimitis,  due  to  bacteria  and  their  toxins,  the  thickening  of  the  intima,  by 
cutting  off  the  nutrition  of  the  inner  layers  of  the  media,  may  weaken  that 
coat,  and  so  cause  a  local  dilatation  of  the  aortic  lumen,  followed  by  a 
secondary  and  further  thickening  of  the  intima;  but  it  is  also  possible  that 
the  infective  endoaortitis  which  undoubtedly  exists  has  no  direct  associa- 
tion with  the  general  process  here  described,  and  that  when,  after  typhoid 
and  other  infections,  there  develops  a  premature  arterio-sclerosis,  here, 
again,  we  deal  with  a  primary  sporadic  degeneration  of  the  media,  set  up 
by  bacterial  toxins. 

3.  The  affection  of  the  media  may  be  either  a  primary  degeneration 
without  signs  of  preceding  inflammation,  or  may  be  of  inflammatory  ori- 
gin (as  in  syphilis). 

4.  The  intimal  change  secondary  to  the  medial  degeneration  has  none 
of  the  features  of  an  extension  of  the  morbid  process  from  the  media,  but  is 
of  a  wholly  different  nature.  It  is  primarily  of  hyperplastic  type — a 
simple  connective-tissue  hyperplasia  unaccompanied  by  the  phenomena 
which  we  associate  with  inflammation. 

Arterio-sclerotic  changes  in  the  aorta  due  to  syphilis  has  been  described 
under  the  heading,  "Syphilitic  Aortitis. "  In  this  type  of  the  disease  the 
puckered,  rubbery  appearance  of  the  lesions  are  characteristic. 

When  the  arterio-sclerosis  is  purely  senile  in  origin  the  heart  may  show 
no  hypertrophy  or  at  best  but  slight  enlargement.  In  the  other  forms  of 
arterio-sclerosis  extreme  hypertrophy  of  the  heart  is  a  very  common  con- 
dition, especially  in  relatively  young  individuals  with  associated  renal 
changes  and  an  abnormally  high  blood-pressure. 

Symptoms. — Atheroma  of  the  thoracic  aorta  alone  rarely  manifests  it- 
self in  the  early  stages  either  by  symptoms  or  physical  signs,  unless  the 
exciting  cause  is  the  spirochete  pallida.  Occasionally,  however,  non- 
specific sclerosis  of  the  thoracic  aorta,  especially  when  the  process  is 
diffuse,  is  attended  with  a  vascular  crises.  In  cases  of  this  type  there  may 
be  substernal  pain,  which  at  times  assumes  the  character  of  angina,  pal- 
pitation of  the  heart  and  marked  dyspnea.  These  symptoms  are  apt  to  be 
precipitated  or  increased  by  physical  exertion.  Attacks  of  this  kind  are 
analogous  to  those  sometimes  occurring  in  the  abdomen  as  the  result  of 
diffuse  atheroma  of  the  abdominal  aorta  or  its  branches  and  in  the 
arteries  of  the  lower  extremities,  the  latter  attacks  being  known  as  inter- 
mittent claudication. 

In  the  majority  of  cases  of  atheroma  of  the  ascending  portion  and 
arch  of  the  aorta  the  process  is  part  of  a  general  arterio-sclerosis  and  the 
symptoms  are  indicative  of  a  general  rather  than  a  local  process. 

The  early  manifestations  of  arterio-sclerosis  are  as  a  rule  indefinite  and 
gradual  in  their  development.  Among  the  premonitory  symptoms  are 
attacks  of  indigestion,  transient  attacks  of  faintness,  headaches,  irritabil- 
ity of  temper,  defects  of  memory,  exhaustion  after  mental  or  physical 
exertion  and  cramps  in  the  muscles  of  leg.  While  in  no  way  pathogno- 
monic the  occurrence  of  such  symptoms  in  an  individual  approaching  or 
just  past  early  middle  life,  should  lead  to  a  thorough  investigation  of  the 
cardio-vascular  system. 

The  constitutional  symptoms  of  arterio-sclerosis  vary  greatly  with  the 
general  make-up  of  the  individual.  In  some  patients  there  is  pallor,  loss 
of  weight  and  a  loose  flabby  skin;  in  others  the  individual  is  stout  and  if  of 
a  gouty  diathesis  there  may  be  a  florid  complexion. 


DISEASES    OF    THE    AORTA  727 

The  manifestations  of  arteriosclerosis  are  not  uniform.  In  some 
cases  there  is  a  gradual  deterioration  of  health;  in  others  the  cardiac 
phenomena  predominate;  in  another  group  the  clinical  picture  is  that  of 
chronic  nephritis;  in  still  others  the  symptoms  may  be  entirely  cerebral  in 
origin ;  finally,  a  chronic  bronchitis  and  emphysema  may  stand  out  most 
prominently. 

While  cardiac  hypertrophy  is  not  always  present,  the  increased  work 
put  upon  the  heart  in  overcoming  the  resistance  in  the  stiffened  arteries 
or  abnormally  high  blood-pressure  without  marked  arterial  changes 
frequently  lead  to  that  condition.  As  in  hypertrophy  due  to  other  causes 
dilatation  of  the  heart  may  occur.  If  the  patient  is  seen  first  at  this  stage 
the  presence  of  dyspnea  and  cyanosis,  together  with  the  signs  of  broken 
compensation  and  a  mitral  murmur  of  relative  insufficiency,  will  likely 
lead  to  a  diagnosis  of  cardiac  failure  clue  to  myocarditis  or  chronic  valvular 
disease. 

The  association  of  sclerosis  of  the  coronary  arteries  and  angina  pectoris 
is  well  known.  Occasionally  an  obliterative  endarteritis  involving  the 
coronary  vessels,  and  without  symptoms  of  angina,  is  the  only  lesion 
which  will  explain  cases  of  sudden  death. 

When  the  kidneys  are  extensively  involved,  the  predominant  symptoms 
are  those  of  a  chronic  contracted  kidney.  In  such  cases  the  daily  out- 
put of  urine  is  increased  and  nocturnal  micturition  is  common.  Pallor 
is  marked  and  while  there  is  puffiness  about  the  eyes  edema  is  not  marked 
in  other  parts  of  the  body.  Examination  of  the  urine  will  show  varying 
traces  of  albumin  and  the  presence  of  hyaline  and  finely  granular  casts. 
It  is  to  be  borne  in  mind  that  the  albumin  and  casts  may  be  intermittently 
present  and  that  for  varying  periods  the  urine  may  show  nothing  more 
than  an  abnormally  low  specific  gravity. 

When  the  cerebral  symptoms  predominate,  there  may  be  attacks 
of  vertigo  or  a  transient  hemiplegia  or  aphasia.  The  latter  are  usually 
of  brief  duration  and  while  recovery  is  complete  recurrences  are  apt  to 
occur. 

It  is  thus  evident  that  the  clinical,  picture  of  chronic  aortitis  varies 
according  to  whether  the  process  is  confined  to  the  aorta  alone  or  is 
associated  with  a  lesion  of  the  aortic  valves,  aneurism,  nephritis  or  a 
general  arterio-sclerosis.  As  an  isolated  lesion  it  often  gives  no  evi- 
dence of  its  existence,  attention  being  directed  to  the  aorta  through 
an  attack  of  acute  aortitis  or  what  Dieulafoy  terms  borrowed  symptoms, 
namely,  those  produced  by  hypertrophy  of  the  heart,  aortic  insufficiency, 
aneurism  or  nephritis. 

Physical  Signs. — While  it  is  the  exceptional  case  of  chronic  aortitis 
that  manifests  itself  by  symptoms,  a  considerable  proportion  of  cases 
can  be  recognized  through  the  physical  findings. 

Inspection. — Although  the  sclerotic  process  may  be  confined  to  the 
thoracic  aorta  it  is  more  commonly  a  part  of  a  general  process  involving 
the  entire  arterial  tree.  In  a  well-marked  case  the  temporal  arteries 
are  seen  to  stand  out  prominently  and  are  often  tortuous.  The  brachials 
are  also  prominent,  often  kinked  and  pulsate  strongly.  If  the  aorta  is 
dilated,  a  valuable  diagnostic  sign  is  pulsation  in  the  suprasternal  notch. 
In  addition  the  right  subclavian  artery  may  be  seen  to  pulsate  above  the 
clavicle,  being  lifted  up  as  a  result  of  the  dilatation  of  the  aorta.  Arcus 
senilis  is  often  noted  in  those  of  advanced  years  and  at  one  time  was  con- 


728  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

sidered  as  being  an  indication  of  sclerosis.  The  condition  is  due  to 
colloidal  degeneration  of  the  superficial  layers  of  the  cornea.  It  is  not 
infrequently  seen  in  those  relatively  young  and  is  quite  common  in 
negroes. 

Inasmuch  as  hypertrophy  of  the  heart  is  so  frequently  associated  with 
arterio-sclerosis,  the  cardiac  impulse  may  be  forcible  and  heaving  in  char- 
acter with  the  apex  beat  displaced  downward  and  to  the  left.  Hyper- 
trophy of  the  heart  furnishes  valuable  evidence  as  to  which  portion  of  the 
arterial  system  is  diseased  or  at  least  most  involved.  Thus  arterio- 
sclerosis leads  to  a  hypertrophy  of  the  left  ventricle  only  when  the  splanch- 
nic arteries  or  the  aorta  above  the  diaphragm  are  highly  diseased. 
The  hypertonicity  or  arterio-sclerosis  of  the  remaining  vascular  districts 
does  not  appear  to  exert  this  influence  (T.  C.  Janeway). 

If  the  renal  symptoms  predominate,  pallor  is  apt  to  be  a  marked 
feature  and  there  may  be  evidences  of  edema.  The  latter  is  usually 
slight;  it  may  manifest  itself  by  puffiness  beneath  the  eyes  and  by  slight 
swelling  of  the  feet  and  tissues  over  the  front  of  the  tibia  (pretibial 
edema) . 

There  are  two  invaluable  aids  in  determining  the  existence  and  degree 
of  severity  of  arterio-sclerosis,  namely,  direct  inspection  of  the  eye  grounds 
with  the  ophthalmoscope  and  the  use  of  the  sphygmomanometer.  Prior 
to  the  introduction  and  perfection  of  these  methods  of  diagnosis  the 
early  stages  of  arterio-sclerosis  usually  passed  unnoticed  and  the  condi- 
tion was  not  recognized  as  such  until  the  symptoms  were  well  marked  and 
the  arteries  had  become  both  visibly  and  palpably  thickened.  Once 
the  disease  has  become  well  advanced,  there  is  little  that  can  be  done; 
on  the  other  hand,  if  it  is  detected  in  its  incipiency,  the  process  frequently 
can  be  arrested.  It  is  for  this  reason  that  the  slightest  of  untoward 
symptoms  occurring  in  individuals  approaching  early  middle  life  should 
excite  suspicion.  Some  observers  advise  that  periodic  examinations  of 
the  urine  and  blood-pressure  be  made  in  individuals  of  or  approaching 
middle  life  in  order  to  detect  the  degenerative  changes  in  their  incipiency. 

It  is  to  be  deplored  that  the  ophthalmoscope  is  not  employed  more 
generally  by  the  internist  who,  if  he  cannot  expect  to  become  an  expert 
with  the  instrument,  can  at  least  acquire  sufficient  skill  to  distinguish 
an  abnormal  from  a  normal  eye  ground. 

The  relation  of  the  retinal  vessels  to  arterio-sclerosis  and  nephritis 
is  so  important  that  even  a  suspicion  of  either  should  lead  to  an  ophthal- 
moscopic examination.  Largely  as  a  result  of  the  studies  of  Marcus 
Gunn  it  has  been  shown  that  the  retinal  vessels  present  a  characteristic 
appearance  in  arterio-sclerosis  and  that  alterations  in  these  vessels 
often  can  be  detected  prior  to  changes  elsewhere  in  the  arterial  system. 

Retinal  arteries  which  have  undergone  sclerotic  changes  show  undue 
tortuosity,  alterations  in  their  size  and  caliber  and  also  present  a  beaded 
appearance.  In  addition  whitish  stripes  are  seen  in  the  arterial  wall 
and  there  is  a  loss  of  translucency  so  that  it  is  impossible  to  see,  as  is 
possible  in  normal  state,  through  the  artery  an  underlying  vein  at  the 
point  of  crossing. 

The  retinal  veins  are  also  tortuous  and  show  alternate  contractions 
and  dilatations;  and  of  even  more  importance  is  the  indentation  of  the 
vein  and  impeding  of  the  venous  circulation  where  a  diseased  artery 
crosses  it. 


DISEASES    OF    THE    AORTA 


729 


The  retina  itself  may  be  slightly  edematous,  grayish  opaque  or  show 
the  presence  of  linear  extravasations  of  blood  along  the  course  of  the 
vessels  or  scattered  roundish  infiltrations  over  the  fundus. 

De  Schweinitz  states  that  the  above-described  changes  may  be  the 
forerunner  of  sclerosis  of  the  cerebral  arteries  and  the  only  indication  that 
such  a  condition  is  present. 

Prior  to  the  introduction  of  the  sphygmomanometer  the  question 
of  whether  arterial  tension  was  increased  or  not  was  determined  largely 
by  the  sense  of  touch.  We  have  all  learned  to  appreciate  how  fallacious 
such  observations  are  and  how  frequently  a  supposedly  high  tension  is 
in  reality  normal  or  vice  versa. 

The  determination  of  what  constitutes  a  normal  tension  standard 
for  the  different  age  periods  is  somewhat  arbitrary.  Woley1  gives  the 
following  results : 


Systolic  blood  pressure 


Age 


High 

Low 

Average 

141 

103 

122 

143 

107 

127 

146 

113 

130 

149 

115 

132 

153 

120 

138 

15-30  years 
30-40  years 
40-50  years 
50-60  years 
60-65  years 


The  diastolic  pressure  is  from  20  to  40  mm.  lower  than  the  systolic. 
In  women  the  systolic  pressure  is  from  8  to  10  mm.  lower  than  in  men 
at  corresponding  age  periods.  It  is  to  be  borne  in  mind  that  the  pressure 
may  be  raised  abnormally  as  the  result  of  physical  exertion,  mental 
activity  and,  especially,  excitement. 

The  fact  that  the  blood-pressure  tends  to  rise  with  advancing  years 
must  not  be  lost  sight  of.  A  systolic  pressure  of  150  mm.  may  be  entirely 
consistent  with  good  health  in  an  individual  of  sixty  years  of  age;  the 
same  pressure  at  thirty  would  be  of  the  most  serious  import. 

A  constant  systolic  pressure  of,  or  above,  160  mm.,  or  a  diastolic  pres- 
sure of  or  above  100  mm.  Hg.  is  pathologic  at  any  age.  The  diastolic 
pressure  is  a  more  active  criterion  of  the  actual  average  pressure  than  is  the 
systolic,  since  it  is  much  less  subject  of  functional  or  emotional  liability. 

While  thickening  of  the  superficial  arteries,  high  blood-pressure,  en- 
largement of  the  left  ventricle  and  a  ringing  second  aortic  sound  form  a 
frequent  combination  in  arterio-sclerosis,  it  not  infrequently  happens  that 
the  pressure  is  not  abnormally  raised.  This  may  be  due  to  poor  nutrition, 
cardiac  weakness,  or  degenerative  changes  in  the  arterioles. 

Whenever  the  systolic  pressure  is  markedly  high,  200  mm.  or  over, 
there  is  always  a  strong  probability  that  the  kidneys  are  diseased,  al- 
though among  the  well-to-do  exceedingly  high  pressures  are  not  infrequent 
and  may  occur  without  evident  arterial  thickening  or  nephritis.  It  is  in 
this  type  of  individual  that  the  sphygmomanometer  is  most  serviceable. 

Percussion. — Hypertrophy  of  the  heart  is  indicated  by  some  extension 
of  the  cardiac  dulness  both  to  the  right  and  left.     In  some  instances  there 

1  Jour.  Am.  Med.  Assoc,  1910,  iv,  121. 


730  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

will  be  an  increase  in  the  area  of  dulness  due  to  dilatation  of  the  aorta. 
At  the  level  of  the  second  costal  cartilage  the  underlying  aorta  normally 
gives  rise  to  a  transverse  area  of  dulness  from  2  to  2^  in.  (4.5  to  5.5  cm.) 
in  width.  If,  therefore,  the  dulness  extends  beyond  these  limits,  especially 
to  the  right  of  the  sternum,  dilatation  of  the  aorta  should  be  suspected. 

Auscultation. — The  most  common  auscultatory  findings  in  cases  of 
chronic  aortitis  are  the  presence  of  a  systolic  murmur  at  the  second  aortic 
cartilage  and  a  sharply  accentuated,  high-pitched,  second  aortic  sound. 
A  systolic  murmur  at  this  area  is  a  very  common  occurrence  and  is  fre- 
quently attributed  to  stenosis  of  the  aortic  outlet.  There  is  probably  no 
more  common  mistake  in  the  diagnosis  of  cardiac  murmurs,  in  spite  of  the 
fact  that  aortic  stenosis  is  recognized  as  the  rarest  of  left-sided  lesions 
(see  p.  685). 

A  systolic  murmur  independent  of  disease  of  the  aortic  valves  may 
be  caused  by  changes  in  the  first  part  of  the  aorta.  The  vessel  may  be 
dilated  or  its  inner  surface  may  be  roughened  by  calcareous  plates  or  the 
artery  may  be  converted  into  a  narrow,  rigid  tube.  In  case  the  vessel  is 
dilated,  the  blood  current  may  be  thrown  into  swirls  thus  giving  rise  to  a 
murmur ;  if,  on  the  other  hand,  the  inner  surface  of  the  vessel  is  roughened 
or  the  artery  is  rigid  the  propulsion  of  the  blood  stream  over  the  rough- 
ened surface  or  through  the  rigid  tube  may  also  produce  a  murmur,  systolic 
in  time.  The  conditions  just  mentioned  are  very  commonly  present  as 
part  of  a  general  arterio-sclerosis,  hence  the  frequency  of  this  murmur. 
Of  almost  equal  importance  is  the  sharply  accentuated,  ringing  character 
of  the  second  aortic  sound. 

In  a  much  smaller  proportion  of  cases  a  diastolic  murmur  is  present. 
"When  this  is  the  case  the  lesion  is  usually  syphilitic  in  origin.  The  mur- 
mur may  be  produced  in  one  of  two  ways:  (1)  A  syphilitic  aortitis  may 
extend  and  involve  the  aortic  valves,  thus  giving  rise  to  an  organic 
valvular  lesion ;  (2)  the  aorta  may  become  dilated  as  the  result  of  a  mesa- 
ortitis  and  in  this  way  the  aortic  ring  may  become  dilated  without  there 
being;  anv  actual  disease  of  the  leaflets  themselves. 


CHAPTER  XXXI 

ANEURISM  OF  THE  THORACIC  AORTA 

An  aneurism  may  be  defined  as  any  circumscribed  or  localized  expan- 
sion or  dilatation  of  the  lumen  of  an  artery. 

If  the  wall  of  the  distended  portion  is  composed  of  all  or  any  of  the 
coats  of  the  artery,  the  aneurism  is  called  "true";  if  the  sac  in  part  or  in 
its  entirety  is  formed  by  surrounding  tissues  or  a  newly  formed  fibrous 
investment,  the  condition  is  spoken  of  as  a  "false"  aneurism. 

An  aneurism  is  almost  invariably  secondary  to  some  disease  of  the 
artery,  such  as  atheromatous  degeneration  or  syphilis.  Occasionally  an 
aneurism  may  arise  in  a  healthy  artery  as  the  result  of  a  sudden  straining 
of  the  wall  whereby  the  intima  is  ruptured;  as  the  result  of  a  wound;  or  as 
the  result  of  the  wall  becoming  eroded  by  the  extension  of  an  inflamma- 
tory process  from  some  adjacent  structure.  Syphilis,  however,  is  to  be 
looked  upon  as  the  most  important  factor  in  the  causation  of  aneurism 
of  the  thoracic  aorta. 

1.  Dilatation  of  the  Aorta. — A  slight  enlargement  of  the  lumen  of  the 
aorta  is  a  relatively  common  condition.  It  constitutes  what  may  be 
termed  an  incipient  form  of  the  disease  and  is  very  commonly  overlooked 
during  life. 

Dilatation  of  the  aorta  may  range  from  a  slight  increase  in  the  diame- 
ter of  the  lumen  of  the  vessel  up  to  an  extreme  degree  of  distention.  It  is 
met  with  most  frequently  in  the  ascending  portion  of  the  arch.  In  this 
situation  the  vessel  presents  a  fusiform  or  cylindrical  dilatation,  the  diame- 
ter being  increased  from  the  normal  5  to  5)4  cm.  to  from  6  to  9  cm.  or  even 
more. 

2.  Saccular  Aneurism. — When  one  speaks  of  an  aneurism  of  the  arch 
of  the  aorta  it  is  the  saccular  variety  that  is  meant  in  the  great  majority  of 
cases.  It  is  this  type  that  is  defined  as  being  a  pulsating  tumor  contain- 
ing blood  in  direct  communication  with  the  interior  of  the  artery.  It  is 
caused  by  the  bulging  or  giving  away  of  a  portion  of  the  arterial  wall  which 
has  been  weakened  by  disease  or,  rarely,  by  injury.  It  differs  from  dilata- 
tion of  the  aorta  in  that  it  is  due  to  a  circumscribed  bulging  at  one  point 
and  not  to  a  stretching  or  distention  of  the  entire  circumference  of  the 
artery. 

3.  Dissecting  Aneurism. — Instead  of  a  localized  bulging  at  the  point 
where  the  intima  is  destroyed  by  disease,  the  blood  may  tear  its  way  be- 
tween the  intima  and  media  for  some  distance  giving  rise  to  what  is  known 
as  a  dissecting  aneurism.  At  some  point  farther  along  the  course  of  the 
artery  it  may  again  rupture  through  the  media  and  communicate  with  the 
interior  (see  Fig.  172). 

4.  Arterio-venous  Aneurism. — This  form  is  rare  in  the  aorta.  Occa- 
sionally, however,  the  aneurismal  sac  may  rupture  into  the  superior  vena 
cava  or  pulmonary  artery,  constituting  what  is  known  as  an  aneurismal 
varix.     Instead  of  rupturing  directly  into  the  vein  there  may  be  a  rupture 

731 


732  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

of  the  aortic  aneurism  with  the  formation  of  a  hematoma  or  false  aneurism ; 
later  rupture  into  the  vein  may  occur.  When  a  false  aneurism  lies  be- 
tween the  opening  in  the  artery  and  that  in  the  vein,  the  condition  is 
spoken  of  as  a  varicose  aneurism. 

5.  False  Aneurism. — If  all  three  coats  of  the  artery  are  torn  or  de- 
stroyed by  disease,  the  blood  escapes  and  forms  a  hematoma.  This  may 
be  walled  off  by  the  surrounding  structures  or,  if  gradually  formed,  a 
fibrous  envelope  may  form.  A  false  aneurism  may  be  caused  by  rupture 
of  the  wall  of  a  diseased  artery  or  the  artery  may  be  healthy,  the  opening 
being  caused  by  a  wound  or  by  erosion  as  the  result  of  disease  in  an  ad- 
jacent structure. 

Etiology. — The  cause  of  an  aneurism  is  alwaj^s  to  be  sought  in  a 
primary  disease  of  the  vessel  wall,  which  weakens  its  resistance  to  the 
blood-pressure.  With  the  possible  exception  of  trauma,  the  same 
factors  which  cause  arterio-sclerosis  also  favor  the  origin  of  aneurism. 

While  any  of  the  acute  infectious  diseases  may  cause  arterial  degen- 
eration, such  an  occurrence  is  not  common  except  in  syphilis.  As  a 
predisposing  factor  in  the  causation  of  aneurism  syphilis  easily  holds 
first  place.  It  has  always  been  acknowledged  that  the  role  played  by 
lues  was  an  important  one.  Now  that  we  have  come  to  recognize  the 
existence  of  a  syphilitic  aortitis  the  percentage  of  cases  due  to  syphilis 
has  materially  increased  and  at  the  present  time  it  is  estimated  that  from 
70  to  85  per  cent,  of  all  aortic  aneurisms  are  to  be  attributed  to  this  cause. 
When  an  aneurism  occurs  in  an  individual  under  forty  it  is  almost  certain 
that  a  luetic  infection  is  the  cause. 

Occasionally,  certain  of  the  other  infections  such  as  pneumonia 
and  erysipelas  may  produce  a  localized  mesaortitis,  thus  leading  to  a 
weakening  of  the  arterial  wall.  Or  an  endocarditis  occurring  in  the  course 
of  acute  rheumatic  fever,  pneumonia  or  septicemia  may  extend  to  the 
aorta  and  as  the  result  of  inflammatory  changes  in  the  intima  weaken 
the  wall  of  the  vessel. 

While  a  very  marked  degree  of  arterial  degeneration  may  be  caused 
by  lead,  alcohol,  tobacco,  gout  and  chronic  nephritis,  aneurism  is  not 
of  verjr  frequent  occurrence  as  the  result  of  these  poisons. 

Next  to  the  presence  of  an  aortitis  the  most  important  factor  in  the 
production  of  an  aneurism  is  internal  strain.  If  the  vessel  wall  has 
become  markedly  diseased  it  may  be  unable  to  resist  the  strain  of  a 
normal  blood-pressure.  In  most  cases  of  aneurism,  however,  the  artery 
has  been  subjected  to  a  severe  strain  such  as  occurs  with  sudden  or 
violent  muscular  effort.  This  is  indicated  by  the  fact  that  a  very  high 
percentage  of  the  cases  having  an  aneurism  have  followed  an  occupation 
which  demanded  great  muscular  exertion,  either  prolonged  or  sudden. 
Thus  stevedores,  iron  workers,  draymen,  soldiers  and  sailors  are  espe- 
cially liable  to  the  disease.  Furthermore,  the  aneurism  is  most  apt 
to  develop  in  the  active  periods  of  life  when  the  muscular  strength  and 
activity  of  the  individual  are  at  their  highest  point.  Any  sudden 
exertion,  such  as  running  upstairs,  straining  at  stool  or  lifting  is  apt  to 
produce  a  sudden  rise  in  the  blood-pressure  and  if  there  is  present  a 
patch  of  mesaortitis  this  sudden  strain  may  cause  the  intima  over  the 
diseased  area  to  split. 

Passive  dilatation  of  the  aorta  may  be  produced  by  persistent  arterial 
hypertension  such  as  occurs  in  chronic  Blight's  disease.     In  this  way  the 


ANEURISM    OF    THE    THORACIC    AORTA  733 

diameter  of  the  ascending  portion  of  the  arch  may  be  increased  up  to 
8  to  9  cm. 

Among  the  rarer  causes  of  aneurism  may  be  mentioned  infective 
emboli.  In  the  large  arteries  septic  emboli  may  lodge  in  the  vasa- 
vasorum  and  produce  a  point  of  suppuration;  later  the  overlying  intima 
ruptures  and  in  this  way  an  aneurism  may  be  formed.  Other  explana- 
tions of  these  mycotic  aneurisms  are  that  there  may  be  an  extension  of  an 
inflammatory  process  from  a  neighboring  infectious  process;  that  there 
may  be  a  metastatic  deposition  upon  the  intima  from  a  valvular 
endocarditis;  and  that  the  surface  of  the  intima  may  become  infected 
from  a  distant  focus. 

A  violent  blow  on  the  chest  or  the  jar  of  a  fall  may  fracture  the 
intima  and  produce  a  dissecting  aneurism.  Finally,  an  aneurism  may 
be  caused  by  the  wall  becoming  weakened  as  the  result  of  some  external 
injury  such  as  a  bullet  or  knife  wound  or  by  disease  of  an  adjacent  organ. 

It  is  evident  from  the  above  facts  that  aneurism  is  practically  always 
secondary  to  arterio-sclerosis  of  the  aorta;  that  syphilis  is  the  most  com- 
mon cause  of  the  arterial  degeneration;  and  that,  in  addition  to  disease 
of  the  vessel,  arterial  strain,  usually  suddenly  produced,  is  an  essential 
factor. 

For  the  reasons  just  given  aneurism  is  usually  encountered  between 
the  ages  of  thirty  and  fifty  when  muscular  activity  is  at  its  height. 
Aneurism  may  occur  at  any  age  but  is  unusual  in  the  very  young  and  the 
very  old.  Typical  aneurisms  have  been  noted,  however,  in  children 
three  or  four  years  of  age;  commonly  there  is  a  history  of,  or  the  evi- 
dences of,  congenital  syphilis. 

Men  are  more  frequently  affected  than  women — in  the  proportion 
of  about  5  to  1.  This  is  due  to  the  fact  that  men  are  more  often  infected 
with  syphilis  and  are  in  addition  engaged  in  laborious  occupations. 
The  incidence  of  aneurism  among  negroes  is  high,  from  two  to  three  times 
as  often  as  among  the  whites.  In  the  vast  majority  of  negroes  suffering 
from  aneurism  syphilis  is  the  cause.  In  the  post-mortem  room  aneurism 
of  the  thoracic  aorta  is  encountered  in  less  than  1  per  cent,  of  cases. 
Lemann1  found  1  in  300,  Osier2  1  in  100  and  Borowsky3  66  among  19;646 
autopsies  (0.34  per  cent.). 

Morbid  Anatomy. — Except  in  case  of  trauma,  which  is  rare,  the  first 
step  toward  the  formation  of  an  aneurism  is  the  development  of  an 
endarteritis;  and  particularly  that  form  which  is  caused  by  syphilis 
(see  Fig.  396).  Chronic  endarteritis  which  terminates  in  widespread 
atheromatous  changes  of  the  aorta  is  of  common  occurrence  without 
aneurism.  On  the  other  hand,  circumscribed  or  focal  lesions,  such  as 
occur  in  syphilis,  are  extremely  liable  to  lead  to  dilatation  or  bulging 
of  the  affected  part  of  the  vessel  wall. 

As  a  rule  the  aneurism  is  a  late  manifestation  of  syphilis.  Winternitz4 
has  reported  a  case  which  shows  an  aneurism  in  its  incipiency  with 
the  minute  sac  extending  through  the  acutely  broken  and  necrotic 
media  to  the  adventitia.  This,  he  believes,  indicates  that  the  aneurism 
may  form  in  the  acute  stage  of  syphilis. 

1  Am.  Jour.  Med.  »S'c,  August,  1910. 

2  Schorstein  Lectures. 

3  Inaugural  Dissertation,  Breslau,  1910. 

4  Bull.  Johns  Hopkins  Hospital,  July,  1913. 


734  DISEASES    OF    THE    PERICARDIT3I,    HEART,    AND    AORTA 

An  aneurism,  is  apt  to  develop  under  the  following  conditions:  The 
aorta,  most  frequently  the  ascending  portion  of  the  arch,  becomes  the 
seat  of  a  syphilitic  aortitis.  This  lesion  either  weakens  or  destroys  the 
media  and  inasmuch  as  the  middle  or  elastic  coat  of  the  artery  consti- 
tutes it's  real  strength,  a  point  of  lowered  resistance  is  established.  If 
a  sufficiently  large  area  of  the  media  is  destroyed  the  vessel  may  dilate 
or  bulge  as  the  result  of  the  strain  of  a  normal  blood-pressure.  In  the 
majority  of  the  cases,  as  we  have  pointed  out  in  the  etiology,  the  occupa- 
tion of  the  individual  is  such  that  the  weakened  wall  is  subjected  to 
an  extra  strain  -because  of  a  sudden  elevation  of  the  blood-pressure 
due  to  muscular  effort.  As  a  result  of  repeated  strains  of  this  sort 
the  weakened  point  gradually  stretches  or  the  intima  overlying  the  patch 
of  mesaortitis  may  tear  and  hasten  the  formation  of  an  aneurism. 

If  the  entire  circumference  of  the  artery  is  diseased,  the  aorta  usually 
undergoes  dilatation,  cylindrical  or  fusiform  in  shape.  The  extent 
of  the  dilatation  varies  greatly;  it  may  be  very  slight  or  it  may  be  so  ex- 
treme as  to  constitute  a  true  aneurism.  Passive  dilatation  may  occur 
as  the  result  of  a  persistently  high  blood-pressure. 

The  most  common  type  is  that  form  in  which  the  artery  gives  way 
at  one  side,  constituting  a  bulging  sac.  As  the  aneurism  increases  in 
size  the  mouth  of  the  sac  becomes  relatively  small  in  comparison  with 
the  interior,  the  blood  current  in  the  sac  becomes  sluggish  and  a  laminated 
clot  is  formed. 

The  rapidity  with  which  the  aneurism  grows  depends  to  some  extent 
on  the  formation  of  a  firm  clot  within  the  sac  and  the  extent  of  the  inflam- 
matory reaction  set  up  in  the  surrounding  tissues,  the  latter  tending  to 
form  a  fibrous  barrier  about  the  tumor.  As  a  rule,  however,  efforts 
toward  arresting  the  increase  in  the  size  of  the  aneurism  are  futile 
unless  the  interior  of  the  sac  can  be  obliterated.  As  long  as  the  mouth 
of  the  sac  remains  open,  each  succeeding  systole  tends  to  increase  the  strain 
on  the  weakened  wall.  The  introduction  of  gold  wire  into  the  sac  is  done 
with  the  idea  of  aiding  in  the  .formation  of  a  clot  which  will  entirely  fill 
it.  In  small  arteries  the  dilated  portion  ma}^  become  obliterated  by  the 
development  of  a  new  growth  from  the  intima.  In  aneurism  of  the 
large  vessels  spontaneous  healing  rarely  occurs,  although  instances  of  this 
have  been  noted,  even  in  the  thoracic  aorta. 

In  the  saccular  form  of  aneurism  there  is  usually  no  trace  of  either  the 
intima  or  media,  the  wall  being  formed  by  the  thickened  adventitia  or 
outer  coat. 

As  the  aneurismal  tumor  increases  in  size  it  gradually  compresses  the 
surrounding  structures  and  may  lead  to  their  destruction.  The  aneurism 
may  by  pressure  necrosis,  erode  through  one  or  the  other  of  the  main 
bronchi,  the  superior  vena  cava,  the  trachea  or  the  esophagus.  The  most 
striking  result  of  the  eroding  effect  of  an  aneurism,  however,  is  to  be  seen 
in  its  destruction  of  tissues  which  resist  its  advance,  such  as  bone.  Thus 
it  very  commonly  destroys  part  of  the  sternum  and  ribs  as  it  extends 
forward  or,  if  the  descending  aorta  is  involved,  the  vertebra  may  be  de- 
stroyed. Figs.  399,  400,  and  401  show  the  size  a  rapidly  developing 
aneurism  maj^  attain.  An  aneurism  differs  from  other  tumors  in  that  it  is 
expansile  and  it  is  to  this  fact  that  its  destructive  ability  is  probably  due. 
Not  only  does  the  tumor  gradually  increase  in  size  but  in  addition  the 
tissues  with  which  it  is  brought  into  contact  are  subjected  to  an  incessant 


ANEURISM    OF    THE    THORACIC    AORTA  735 

pounding.  Very  often  that  portion  of  the  chest  wall  which  overlies  the 
aneurism  is  destroyed  completely  so  that  nothing  but  the  subcutaneous 
tissues  and  the  skin  remain.  It  is  noteworthy  that  an  aneurism  does 
not  ften  orupture  externally  even  when  nothing  but  the  skin  intervenes. 


Fig.  399. — Aneurism  of  ascending  and  transverse  portion  of  the  arch  of  the  aorta. 

{Pennsylvania  Hospital.) 


Fig.  400. — Aortic  aneurism  a  few  days  before  rupture  into  the  left  bronchus.  The 
oozing  blood  can  be  seen  trickling  down  over  the  lower  part  of  the  sac.  (Pennsylvania 
Hospital.) 

While  an  individual  with  an  aneurism  may  die  from  some  intercurrent 
illness,  in  about  one-half  the  termination  is  death  from  rupture  of  the 
sac.  Many  cases  of  sudden  death  are  clue  to  rupture  of  an  unsuspected 
aneurism. 


736 


DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


Usually  there  is  but  one  aneurism  but  there  may  be  two  or  more  (see 
Fig.  403).  Occasionally  there  are  a  number  of  aneurisms  involving 
different  arteries  throughout  the  body. 

The  aneurism  varies  greatly  in  size.  If  of  the  dilatation  type,  the 
lumen  of  the  vessel  may  be  slightly  increased  or  the  artery  may  be  tre- 
mendously distended  in  the  form  of  a  bag.  In  the  more  common  saccu- 
lated variety  the  bulging  point  varies  from  the  size  of  an  English  walnut 
to  an  enormous  tumor  the  size  of  a  fetal  head. 


p.  A. 


L.A 


T.A 


Fig.  401. — Sagittal  section  of  aortic  aneurism  in  case  shown  in  Fig.  400.  E,  Esopha- 
gus; R,  point  of  rupture  into  right  bronchus  and  esophagus.  Inimediately  above  this  point 
the  bronchus  is  seen  completely  flattened  out,  accounting  for  the  atelectatic  left  lung; 
L.A.,  left  auricle;  T.A.,  thoracic  aorta;  C,  cardiac  end  of  stomach  which  is  filled  with  blood 
clot;  P. A.,  pulmonary  artery. 

The  aneurism  has  eroded  the  sternum  and  except  for  a  small  channel  at  its  posterior 
part  is  filled  with  a  firruly  organized  thrombus. 


Symptoms  of  Aneurism  in  General. — The  clinical  picture  of  thoracic 
aneurism  is  subject  to  a  number  of  variations  depending  largely  on  the 
particular  part  of  the  arch  affected.  For  this  reason  it  seems  best  to 
describe  the  symptoms,  pressure  effects  and  physical  signs  of  aneurism  in 
general  and  then  to  group  these  findings  around  the  various  clinical  types 
of  aneurism  of  which  thev  are  characteristic. 


ANEUEISM    OF    THE    THORACIC    AORTA  737 

Small  aneurisms  involving  the  intrapericardial  portion  of  the  aorta,  and 
including  the  sinuses  of  Valsalva,  are  frequently  of  rapid'  growth  and 
rupture  may  occur  without  there  having  been  any  previous  symptoms 
(Fig.  404).  Then,  too,  an  aneurism  may  attain  considerable  size  in  the 
ascending  aorta  without  causing  symptoms,  although  physical  signs  may 
be  well  marked.     The  mobility  of  this  part  of  the  aorta  and  the  fact  that 


Fig.  402. — Aneurism  of  the  aorta,  hydrothorax,  atelectasis  of  the  left  lung.  The 
atelectasis  resulted  from  pressure  on  the  bronchus;  the  hydrothorax  from  pressure  on  the 
pulmonary  veins  as  shown  in  Fig.  401.  The  frozen  serum  has  been  removed  from  the 
pleural  cavity,  and  the  laminated  clot,  from  the  aneurismal  sac. 

it  is  not  in  very  close  relationship  with  surrounding  structures  may  account 
for  the  absence  of  subjective  symptoms.  On  the  other  hand,  aneurisms 
that  give  rise  to  numerous  and  severe  symptoms  may  not  be  demonstrable 
by  physical  signs;  this  is  quite  apt  to  be  the  case  when  the  aneurism  in- 
volves the  transverse  or  descending  portions  of  the  arch.  This  is  due  to 
the  fact  that  the  transverse  arch  is  so  firmly  fixed  and  in  such  close  rela- 

47 


738  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

tions  with  important  structures  as  the  trachea,  esophagus,  left  bronchus, 
left  recurrent  laryngeal  nerve,  etc.,  that  even  a  small  aneurism  in  this 
situation  is  apt  to  cause  marked  pressure  symptoms. 

The  descending  portion  of  the  arch  is  also  apt  to  manifest  itself  by 
symptoms  rather  than  physical  signs.  Recognizing  these  facts,  Broad- 
bent  divided  thoracic  aneurisms  into  two  classes,  namely,  aneurism  of 
physical  signs  and  aneurism  of  symptoms;  the  former  term  applying  to 
aneurism  of  the  ascending  and  the  latter  to  aneurism  of  the  transverse 
and  descending  portions  of  the  arch. 


Fig.  403. — Large  multiple  aortic  aneurism.     (Courtesy  of  Dr.  H.  K.  Pancoast.) 

As  a  rule  patients  suffering  from  aneurism  are,  when  first  seen,  robust, 
vigorous-looking  young  and  middle-aged  individuals.  In  the  beginning 
the  symptoms  become  noticeable  only  upon  exertion  when  there  may  be 
some  dyspnea,  palpitation  of  the  heart,  a  sense  of  precordial  oppression 
or  actual  pain. 

Pain  is  one  of  the  most  distinctive  features  of  aneurism.  It  may  occur 
as  the  result  of  disease  in  the  aorta  itself  or  it  may  be  due  to  the  pressure  of 
the  growing  tumor.  The  latter  will  be  considered  under  pressure  effects. 
Pain  referable  to  disease  of  the  aorta  may  be  due  to  one  of  two  causes: 
(1)  It  may  be  anginoid  in  character  due  to  involvement  of  the  coronary 
orifices  as  the  result  of  an  aortitis  and  this  pain  may  recur  in  the  form  of 


ANEURISM    OF    THE    THORACIC    AORTA 


739 


attacks  of  true  angina  pectoris.  (2)  Osier  has  called  attention  to  the  fact 
that  many  individuals  at  the  onset  suffer  from  attacks  of  pain  of  the 
greatest  severity,  this  being  due  to  splitting  of  the  intima  over  a  patch  of 
mesaortitis.  Attacks  of  this  character  gradually  disappear  as  the  tumor 
increases  in  size. 

In  about  one-half  of  the  cases  perforation  of  the  aneurism  causes  death 
before  there  has  been  any  marked  deterioration  in  the  general  health. 
When  death  is  not  caused  suddenly  by  perforation,  the  patient  gradually 
fails  in  strength,  the  disease  pursuing  a  course  similar  to  that  seen  in 


Fig.   404. — Aortic  aneurism  (intrapericardial).      (Courtesy  of  Dr.  H.  K.  Pancoast.) 


chronic  heart  disease.  Aortic  insufficiency  is  very  frequently  a  marked 
feature  of  aneurism  and  as  a  result  the  left  ventricle  hypertrophies ;  later, 
when  compensation  fails,  there  develop  marked  dyspnea,  edema  and 
other  evidences  of  cardiac  failure.  In  some  cases  a  severe  secondary 
anemia  develops  as  the  result  of  oozing  from  the  aneurism.  An  unusual 
event  is  perforation  of  the  aneurism  into  the  vena  cava;  death  usually 
occurs  within  a  few  hours  but  the  patient  may  live  for  some  months. 

The  terminal  event  may  be  an  attack  of  pneumonia  or  death  may 
occur  as  the  result  of  compression  of  the  esophagus,  trachea  or  a  main 
bronchus. 

Dieulafoy  has  emphasized  the  importance  of  tuberculosis  as  a  termi- 


740  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

nal  infection  in  cases  of  thoracic  aneurism,  having  noted  it  in  18  of  46  cases 
under  his  observation. 

Pressure  Effects. — Pain. — In  the  majority  of  aneurisms  involving  the 
aorta  pain  is  at  some  time  or  other  a  conspicuous  symptom.  The  char- 
acter of  the  pain  varies  greatly  in  different  cases.  It  may  be  nothing 
more  than  a  transient  feeling  of  substernal  discomfort  or  it  may  be  in  the 
nature  of  persistent  or  recurring  attacks  of  neuralgia.  Keeping  in  mind 
this  fact,  one  should  always  be  alert  to  the  possibility  of  a  thoracic  aneu- 
rism in  individuals  who  complain  of  chest  pain  which  is  not  otherwise 
explainable. 

Pain  produced  by  an  aneurism  in  the  ascending  aorta  is,  as  a  rule,  not 
severe  in  spite  of  the  fact  that  it  erodes  the  sternum  and  ribs.     Pain  is 


Fig.  405. — Aneurism   of   ascending   transverse   and   descending   aorta,    the   latter   being 
adherent  to  the  dorsal  vertebrae  which  were  in  part  eroded  from  pressure. 

more  apt  to  occur  as  the  result  of  an  aneurism  in  this  situation  when  the 
growth  extends  backwards.  It  is  usually  vague  and  not  at  all  severe 
except  when  the  aneurism  is  growing.  The  pain  may  be  increased  or 
relieved  by  different  postures ;  or  it  may  be  referred  to  the  right  shoulder  or 
the  scapular  region.  Spasm  of  the  right  trapezius  muscle  has  been  noted 
also. 

When  the  transverse  portion  is  involved,  the  pain  is  usually  vague  and 
deep-seated.  In  this  situation  the  growth  is  more  apt  to  interfere  with 
the  function  of  the  structures  immediately  surrounding  it  rather  than  give 
rise  to  severe  pain. 

The    most  intense  pain  is  produced  by  an  aneurism  involving  the 


ANEURISM    OF    THE    THORACIC    AORTA  741 

descending  portion  of  the  arch  and  the  descending  thoracic  aorta.  This 
is  due  to  the  close  relation  of  the  spinal  column  and  the  thoracic  aorta 
(Fig.  405).  In  this  situation  erosion  of  the  vertebrae,  the  implication  of 
the  intercostal  nerves  and,  in  some  cases,  the  spinal  cord  often  cause  a 
persistent,  boring  pain  or  sharp,  lancinating  neuralgic  attacks  of  the 
greatest  severity.     The  pain  may  be  the  only  manifestation  of  the  disease. 

Special  Nerves. — Next  to  pain  the  most  common  manifestation  of 
pressure  is  the  involvement  of  certain  special  nerves. 

Left  Recurrent  Laryngeal. — This  nerve,  which  arises  from  the  vagus, 
enters  the  thorax,  passes  around  the  arch  of  the  aorta  and  ascends  in 
the  space  between  the  esophagus  and  trachea.  In  addition  to  supplying 
motor  fibers  to  the  larynx  it  also  sends  branches  to  the  esophagus, 
trachea  and  pharynx.  It  can  be  readily  seen  that  if  the  aneurism  involves 
the  transverse  portion  of  the  arch  there  is  very  apt  to  be  a  disturbance 
of  function  in  the  parts  enervated  by  the  left  recurrent  laryngeal.  If 
the  nerve  is  stimulated,  there  may  be  produced  painful  spasms  of  the 
pharynx,  the  esophagus  or  larynx.  In  addition  there  may  be  difficulty 
in  swallowing  (dysphagia)  or  a  feeling  of  suffocation  due  to  narrowing  of 
the  glottis.  The  nerve  may  be  so  pressed  or  stretched  as  to  cause 
paralysis  of  the  left  vocal  cord ;  in  such  instances  the  voice  may  be  husky, 
cracked  or  tremulous  in  character.  The  so-called  "  brassy"  cough  is  fre- 
quently present  (see  Figs.  92  and  170). 

The  right  recurrent  laryngeal  nerve  does  not  enter  the  thorax  but 
curves  around  .  the  subclavian  artery.  It  is  sometimes  involved  by 
extension  of  the  aneurism  upward  to  the  right  or  as  the  result  of  the 
innominate  also  being  involved. 

Rarely  the  phrenic  nerve  is  implicated.  When  this  occurs  there  may 
be  hiccough  or  even  paralysis  of  the  diaphragm. 

Sympathetic  Nerves. — Inequality  of  the  pupils  in  cases  of  thoracic 
aneurism  may  be"  due  to  several  causes.  Pressure  on  the  sympathetic 
nerves  is  usually  credited  with  being  the  most  common  cause  of  the 
condition.  The  pupil  on  the  affected  side  may  dilate  or  contract  accord- 
ing to  whether  the  sympathetic  fiber's  are  irritated  or  destroyed  by  the 
aneurism.  In  some  instances  the  inequality  may  be  due  to  changes  in 
the  blood-vessels,  compression  or  obstruction  in  the  carotid  causing  a 
dilated  pupil.  .  It  is  to  be  borne  in  mind  that  inasmuch  as  thoracic 
aneurism  is  so  frequently  a  luetic  manifestation,  the  pupillaiy  change 
may  be  specific  in  origin  and  independent  of  the  aneurism ;  when  a  mani- 
festation of  syphilis,  the  light  reflex  is  lost,  whereas  in  cases  of  aneurism 
the  sensitiveness  to  light  is  retained. 

Esophagus. — Difficulty  in  swallowing  may  be  transient  or  persistent. 
When  transient,  it  is  usually  due  to  spasm  resulting  from  irritation  of  the 
recurrent  laryngeal  nerve;  when  persistent,  it  is  due  to  direct  pressure 
of  the  aneurism  (see  Fig.  401).  This  may  occur  when  either  the  trans- 
verse or  descending  portions  of  the  arch  are  involved;  it  is  occasionally 
noted  in  aneurisms  of  the  descending  thoracic  aorta.  The  pressure  is 
rarely  sufficiently  marked,  however,  to  cause  complete  blocking  of  the 
esophagus  but  there  may  be  sufficient  narrowing  of  the  lumen  to  render 
the  swallowing  of  solid  food  difficult  or  impossible.  In  considering  the 
possibility  of  stricture  of  the  esophagus  the  presence  of  an  aneurism 
must  be  excluded  before  attempting  to  pass  a  stiff  exploring  instrument, 
otherwise  the  growth  may  be  perforated. 


742 


DISEASES    OF   THE    PERICARDIUM,    HEART,    AND    AORTA 


Trachea  and  Bronchi. — When  the  aneurism  occurs  in  the  transverse 
portion  of  the  arch,  pressure  on  the  trachea  is  apt  to  occur.  This  may- 
give  rise  to  a  dry,  brassy  cough ;  there  may  be  in  addition  some  expecto- 
ration which  is  often  blood-streaked.  Dyspnea  may  also  occur.  If 
the  trachea  is  directly  compressed,  there  may  be  little  difficulty  in 
breathing  except  when  the  patient  exerts  himself.  In  some  instances 
the  dyspnea  may  be  paroxysmal  in  character  and  be  so  intense  as  to 
cause  a  feeling  of  suffocation.  These  paroxysmal  attacks  may  be  due 
to  direct  compression  of  the  trachea  or  as  a  result  of  the  left  recurrent 
laryngeal  nerve  being  involved.  More  rarely  one  of  the  main  bronchi 
may  become  compressed  (see  Figs.  401  and  402).  When  either  the 
trachea  or  bronchi  are  involved  there  is  apt  to  be  some  diminution  in 


Fig.  406. — Left  lung  is  greatly  compressed  in  its  upper  part.  Circular  opening  shows 
interior  of  the  aneurism  sac.  Note  large  size  of  aneurism  and  small  size  of  heart.  {Jeffer- 
son Medical  College  Museum.) 

the  intensity  of  the  respiratory  murmur;  this  will  be  bilateral  if  the 
trachea  is  compressed  and  unilateral  if  the  lumen  of  one  of  the  main 
bronchi  is  narrowed. 

The  Lungs.— In  some  instances  one  or  the  other  of  the  lungs  become 
compressed  by  the  aneurismal  sac.  The  lung  immediately  adjacent  to 
the  aneurism  becomes  congested  and  atelectatic  and  may  eventually 
undergo  fibroid  changes.  Bramwell1  has  reported  13  cases  of  aortic 
aneurism  in  which  pressure  at  the  root  of  the  lung  produced  consolida- 
tion or  chronic  pneumonia.     In  8  cases  the  left  lung  was  involved,  in  4 

1  Edinburgh  Med.  Jour.,  xvi,  Xo.  2,  1916. 


ANEURISM    OF   THE    THORACIC    AORTA  743 

the  right.  Tuberculosis  was  present  in  1  case,  side  not  given.  A 
weakened  respiratory  murmur  and  hemoptysis  are  apt  to  result  if 
the  compression  is  at  all  marked  (Fig.  406). 

Veins. — Among  the  most  striking  effects  of  aneurism  is  compression 
of  one  of  the  great  veins.  The  veins  most  likely  to  be  involved  are  the 
inferior  vena  cava,  the  innominates,  the  subclavians  and  the  pulmonary 
veins.  Complete  obliteration  of  the  superior  cava  is  rare  but  a  certain 
amount  of  compression  is  not  unusual.  If  the  compression  occurs  sud- 
denly, it  gives  rise  to  varying  degrees  of  edema  of  the  head,  neck  and  arms 
and  cyanosis  of  the  face.  Rarely  the  larynx  and  pharynx  may  become 
edematous  and  thus  give  rise  to  severe  dyspnea. 

When  the  pressure  is  exerted  gradually,  the  collateral  veins  assume 
much  of  the  burden  and  thus  obviate  the  symptoms  described  above.  But 
even  when  an  adequate  collateral  circulation  is  established,  there  is  very 
apt  to  be  some  congestion  of -the  veins  of  the  head  and  neck  and  some- 
times one  or  other  of  the  arms.  The  jugulars  are  often  distended. 
Distention  of  the  jugulars  under  these  circumstances  is  to  be  distin- 
guished from  that  occurring  in  cases  of  failing  compensation  by  reason  of 
the  fact  that  the  veins  do  not  pulsate  in  cases  of  aneurism. 

The  collateral  circulation  may  be  carried  on  through  the  intercostal  and 
internal  mammary  veins ;  through  the  deep  cervical,  the  vertebrae  and  in- 
tercostal veins;  and  through  branches  of  the  mammary  veins  on  the  sur- 
face of  the  chest.  The  front  of  the  chest  may  be  occupied  by  a  mass  of 
dilated  veins,  some  of  which  are  the  size  of  a  finger.  In  some  instances 
the  veins  are  in  the  subcutaneous  tissue;  in  others  the  veins  of  the  skin 
itself  are  greatly  distended.  As  a  rule,  dilated  veins  are  not  seen  over 
the  lower  part  of  chest  but  occasionally  they  are,  and  in  some  cases  they 
may  extend  over  the  abdomen. 

When  one  or  the  other  of  the  innominate  veins  is  involved  inde- 
pendently of  the  superior  vena  cava,  the  obstruction  manifests  itself 
by  a  one-sided  distention  of  the  veins  of  the  neck.  In  the  same  way 
distention  of  the  veins  of  one  upper  extremity  may  occur  if  the  sub- 
clavian vein  on  that  side  has  been  compressed. 

An  unusual  occurrence  is  pressure  on  the  right  pulmonary  veins. 
This  gives  rise  to  congestion  of  the  lung  and'  later  to  a  hydrothorax 
(Fig.  109).  The  mechanism  is  the  same  as  when  the  distended  right 
auricle  compresses  the  right  pulmonary  veins  and  thus  leads  to  an  effusion. 

Symptoms  of  Rupture. — The  terminal  event  in  about  one-half  of 
the  cases  of  aneurism  is  a  fatal  hemorrhage  due  to  rupture  of  the  sac. 
Lemann1  collected  592  cases  of  thoracic  aneurism  in  which  rupture  oc- 
curred. The  rupture  involved  the  following  structures  respectively  in  the 
order  of  their  frequency:  Pericardium  alone  148,  left  bronchus,  pleura 
or  lung  160,  right  bronchus,  pleura  or  lung  62,  esophagus  50,  trachea  48, 
superior  vena  cava  31,  pulmonary  artery  18,  into  other  structures  40. 
Although  rupture  externally  through  the  skin  is  looked  upon  as  being 
quite  rare,  Lemann  found  35  cases  (5.9  per  cent.)  recorded  in  which 
the  accident  had  occurred. 

The  occurrence  of  hemoptysis  in  association  with  aneurism  is  not 

infrequent.     The  sputum  may  be  blood-streaked  as  the  result  of  an 

erosion  in  the  trachea,  one  of  the  main  bronchi  or  the  lung  itself.     As 

in  the  case  of  rupture  into  other  organs  an  immediately  fatal  hemorrhage 

1  Am.  Jour.  Med.  Sc,  August,  1916. 


744  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

may  result  but  in  some  cases  small  hemoptyses  may  occur  for  days  or 
weeks;  a  few  cases  have  been  recorded  in  which  years  have  elapsed  after 
the  occurrence  of  a  pulmonary  hemorrhage.  Because  of  the  blood  spit- 
ting, cough  and  dulness  at  or  near  one  apex,  tuberculosis  is  often  mis- 
taken for  aneurism. 

Rupture  into  the  great  vessels  and  into  the  heart  will  be  considered 
under  the  heading  "  Arterio-venous  Aneurisms." 

Physical  Signs. — Inspection. — The  value  of  acquiring  a  good  technique 
in  the  examination  of  patients  is  nowhere  more  evident  than  in  those 
suffering  from  aneurism.  The  nature  of  an  external,  pulsating  tumor 
can  be  recognized  at  a  glance,  but  in  the  absence  of  this  mistakes  will 
almost  certainly  occur  if  the  examination  is  not  thorough.  A  proper 
inspection  of  the  patient  is  an  absolute  necessity  and  if  this  procedure  is 
not  carried  out  carefully  and  systematically  the  clue  leading  to  a  correct 
diagnosis  will  often  escape  notice.  "How  many  eyes=--yes,  and  skilled 
eyes,  too — looked  at  the  thorax  and  never  saw  the  so-called  Litten's  sign 
or  diaphragm  phenomenon?  Many  of  us  look  at  it  every  day  and  fail  to 
see  it,  even  after  we  know  about  it.  How  often  does  the  diagnosis  of  a 
thoracic  aneurism  go  begging  for  want  of  a  careful  glance?"  (Thomas 
McCrae).  There  are  two  prime  essentials:  (1)  The  patient  must  be 
stripped  to  the  waist;  and  (2)  there  must  be  a  good  light. 

Inequality  of  the  pupils  is  always  suggestive  of  some  intrathoracic 
mischief  and  should  therefore  be  given  due  consideration.  Some  disturb- 
ance in  the  return  of  the  blood  through  the  superior  cava  or  its  main 
tributaries  may  be  suggested  by  congestion  of  the  face  or  undue  promi- 
nence of  the  veins  in  the  neck  or  upper  extremities.  The  distention  of  the 
veins  may  be  bilateral  or  unilateral.  In  some  cases  the  veins  over  the 
anterior  chest  wall  may  be  distended  also ;  sometimes  to  a  very  marked 
degreee. 

In  addition  to  distention  of  the  veins  one  or  both  of  the  arms  may  be 
swollen  and  congested  or  pallor  and  sweating  may  be  present  in  one  hand 
and  arm  as  the  result  of  pressure  on  the  sympathetic.  In  a  few  instances 
unilateral  swelling,  simulating  clubbing  of  the  fingers,  has  been  noted. 

When  the  chest  itself  is  subjected  to  inspection,  the  patient  must  be 
placed  facing  a  good  light.  The  observer  should  inspect  the  chest  from 
different  positions ;  in  some  cases  a  slight  pulsation  becomes  visible  only 
when  an  oblique  light  falls  on  the  chest  (see  Fig.  116). 

One  of  the  most  important,  if  not  the  most  important,  diagnostic  signs 
of  thoracic  aneurism  is  the  presence  of  a  pulsation  in  the  area  about  the 
base  of  the  heart.  Fig.  407  indicates  the  points  at  which  pulsation  due 
to  aneurism  is  most  frequently  noted.  In  addition,  when  the  descending 
thoracic  aorta  is  involved,  pulsation  may  be  noted  in  the  left  interscapular 
area  or  just  below  the  angle  of  the  left  scapula.  This  serves  to  emphasize 
the  fact  that  a  thorough  inspection  of  the  back  is  as  necessary  as  the  ex- 
amination of  the  front  of  the  chest. 

The  distinctive  feature  of  aneurismal  pulsation  is  that  it  is  expansile  in 
character.  This  is  most  noticeable  when  the  sac  reaches  the  chest  wall 
and  projects  slightly  beyond  the  surface.  But  even  if  the  aneurism  is 
deep-seated  and  does  not  reach  the  chest  wall  the  impulse  which  is  seen 
and  felt  has  a  heaving  and  expansile  quality.  The  impulse  is  systolic  in 
time  and  usually  consists  of  a  single  motion,  but  may  be  heaving  or  un- 
dulatory  in  character.     A  pulsation  due  to  aneurism  is  usually  in  or  just 


ANEURISM  OF.  THE  THORACIC  AORTA 


745 


to  one  side  or  the  other  of  the  median  line.  Osier  gives  the  following 
description  of  impulses  which  might  be  mistaken  for  aneurism:  (1)  The 
throbbing  of  the  conus  arteriosus  in  the  second  left  interspace — very 
common  in  young  persons  and  in  thin  chests,  and  seen  particularly 
well  during  expiration.  (2)  Pulsation  of  the  heart  in  the  second,  third, 
and  fourth  left  interspaces,  extending  as  far  as  the  nipple  in  cases  of 
fibrosis  and  retraction  of  the  upper  lobe  of  the  lung.  (3)  Cardiac  pulsa- 
tion in  the  second,  third  and  fourth  right  interspaces  in  association  with 
fibrosis  and  retraction  of  the  right  upper  lobe.  (4)  Effusion  on  either 
side  of  the  chest  may  so  displace  the  heart  that  there  is  a  marked  impulse 
at  or  outside  the  nipple  line  on  either  side.     (5)  Throbbing  subclavians 


Fig.  407. — Locations  on  the  anterior  chest  wall  at  which  aneurismal  impulses  may  be  noted 

in  their  order  of  frequency. 


seen  in  the  outer  half  of  the  infraclavicular  regions;  this  is  seen  in  thin- 
chested  persons,  in  neurasthenia,  Graves'  disease,  early  tuberculosis  and 
anemia.  In  some  instances,  when  the  pulsation  is  unilateral,  it  may  be 
accompanied  with  a  thrill  and  a  murmur  forming  a  mimic  or  phantom 
aneurism.  (6)  In  the  back  of  the  chest  a  visible  pulsation  is  nearly 
always  aneurismal;  but  occasionally,  in  Broadbent's  sign,  the  tugging  may 
be  so  limited  and  localized  in  one  interspace  that  it  simulates  pulsation, 
but  palpation  easily  corrects  this. 

In  some  cases  of  anemia,  in  Grave's  disease  and  neurasthenia  there  may 
be  a  diffuse  throbbing  over  the  interior  portion  of  the  thorax  or  a  distinct 
systolic  impulse  may  be  noted  in  the  lower  part  of  either  side  of  the  chest. 
A  pulsation  due  to  a  purulent  pleural  effusion  is  occasionally  seen.  It  is 
usually  on  the  left  side  and  occurs  below  and  outside  the  nipple. 


746 


DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


Except  the  pulsation  that  occurs  in  the  back,  the  farther  removed  the 
impulse  is  from  the  areas  shown  in  Fig.  407  the  less  likely  is  it  to  be  due  to 
aneurism  of  the  aorta.  In  association  with  the  impulse  the  ribs  to  the 
right  or  the  left  of  the  sternum  or  the  manubrium  itself  may  project  ab- 
normally as  the  result  of  the  underlying  sac  or  there  may  be  a  distinct 
tumor  if  the  bony  structures  have  become  eroded.  The  skin  over  the 
tumor  may  be  ulcerated  or  may  "sweat"  blood  (Fig.  408). 

The  apex  beat  of  the  heart  is  often  displaced  downward  and  outward, 
partially  as  the  result  of  pressure  and  partially  because  of  cardiac  hyper- 
trophy. The  heart  may,  however,  show  no  enlargement  and  occupy  its 
normal  position  (see  Fig.  406).  The  heart  is  said  not  to  be  enlarged  un- 
less the  aortic  valves  are  incompetent. 


Fig.   408. — Oozing  of  blood  from  aneurism  sac. 


In  every  case  of  suspected  aneurism  the  larynx  should  be  inspected. 
Pressure  or  stretching  of  the  left  laryngeal  nerve  may  lead  to  paralysis  of 
the  abductor  muscles  and  consequently  to  paralysis  of  the  left  vocal 
cord.  As  a  rule  this  leads  to  some  dyspnea  and  alterations  in  the  voice 
but  even  with  the  vocal  cord  fixed  in  the  middle  line,  there  may  be  no 
change  in  the  voice. 

Rarely  the  right  laryngeal  nerve  may  be  involved  and  still  more  rarely 
there  may  be  bilateral  abductor  paralysis. 

Palpation. — Three  important  signs  are  obtained  by  palpation: 

1.  Diastolic  Shock.- — This  is  one  of  the  most  conclusive  signs  of  aneu- 
rism, some  observers  ranking  it  as  the  most  important  single  sign  we 
have.     It  consists  of  a  short,  sharp  impulse  coincident  with  diastole. 

2.  Thrill- — This  is  usually  systolic  in  time ;  rarely  it  is  double  or 
diastolic  alone.  If  the  sac  contains  much  clot,  and  especially  if  the 
anterior  portion  of  the  sac  is  filled,  the  thrill  is  usually  absent.  It  occurs 
more  frequently  in  cases  of  dilatation  of  the  arch  than  in  the  sacculated 
variety  of  aneurism. 


ANEURISM  OF  THE  THORACIC  AORTA  747 

3.  Pulsation.- — If  the  aneurism  has  perforated  the  chest  wall  there  will 
be  imparted  to  the  palpating  hand  an  impulse  which  is  heaving  and  ex- 
pansile in  character.  If  the  pulsation  is  noted  to  be  expansile  there  is 
little  doubt  as  to  the  true  nature  of  the  trouble.  This  may  be  absent, 
however,  if  the  sac  is  filled  with  a  clot.  In  some  cases  the  sac  is  soft  and 
fluctuating  but  usually  it  is  firm  in  consistency.  In  the  early  stages  of 
aneurisms  which  eventually  perforate  and  in  those  which  are  deep-seated 
and  never  appear  externally,  the  impulse  may  be  very  slight.  Bimanual 
palpation  should  always  be  practiced  in  suspected  cases.  One  hand  is 
placed  over  the  base  of  the  heart  and  the  other  over  the  vertebrae  and 
firm  pressure  is  made.  This  will  often  reveal  a  slight  pulsation  which 
would  otherwise  escape  notice.  As  a  rule  the  impulse  is  best  felt  by 
placing  the  palm  of  the  hand  flat  over  the  suspected  area  but  in  some  cases 
the  impulse  can  be  detected  only  by  pressing  the  finger  tips  deep  into  the 
intercostal  spaces.  The  impulse  may  be  felt  only  at  the  end  of  expiration. 
The  throbbing  of  an  aneurism  differs  from  that  felt  over  a  hypertrophied 
heart  in  that  it  is  localized  and  imparts  to  the  palpating  hand  a  heaving 
and  expansile  quality.  In  some  cases  the  impulse  is  felt  only  when  the 
fingers  are  pushed  downward  in  the  suprasternal  notch. 

Tracheal  tugging  or  Oliver's  sign  may  be  elicited  in  cases  of  aneurism 
of  the  transverse  arch  when  the  sac  has  become  adherent  to  the  trachea. 
This  is  apt  to  produce  a  downward  tug  of  the  larynx  with  each  impulse. 
The  sign  may  be  elicited  by  having  the  patient  sitting  or  standing  in  front 
of  the  observer  who  gently  but  firmly  grasps  the  cricoid  cartilage  with 
the  thumb  and  finger  while  the  head  is  slightly  extended.  The  head 
is  then  flexed  and  the  patient  told  to  hold  his  breath.  If  a  tug  is  present, 
the  up-and-down  motion  of  the  larynx  is  transmitted  to  the  observer's 
fingers.  Another  way  of  detecting  this  sign  is  for  the  examiner  to  stand 
behind  the  patient,  steadying  the  latter 's  head  against  his  body.  The 
cricoid  cartilage  is  then  firmly  grasped  by  the  thumb  and  forefinger. 
Instead  of  an  up-and-down  motion  of  the  larynx  there  may  be  a  lateral 
movement.     This  is  known  as  Cardarelli's  sign. 

The  Peripheral  Arteries. — In  most  individuals  suffering  from  aneurism 
the  arteries  are  palpably  thickened,  but  in  young  syphilitic  subjects  the 
arterial  degeneration  may  be  limited  to  the  aorta. 

The  interposition  of  an  aneurismal  sac  between  the  heart  and  the 
peripheral  vessels  may  lead  to  retardation  or  feebleness  of  the  pulse  in 
the  latter.  The  effects  of  the  sac  on  the  pulse  wave  are:  (1)  to  delay  it; 
(2)  to  diminish  its  height ;  (3)  to  cause  its  duration  to  be  longer,  and  the 
subsidence  more  gradual  and  slower  than  normal;  and  (4)  the  artery 
will  also  be  constantly  full  between  beats,  as  the  sac  aets  like  a  black- 
smith's bellows — being,  in  fact,  a  reservoir  of  blood  (Broadbent). 

If  the  sac  is  located  in  the  ascending  portion  of  the  arch,  the  alteration 
in  the  pulse  wave  will  be  the  same  on  both  sides  and  there  is  then  no 
standard  of  comparison,  but  if  the  sac  involves  the  great  vessels  given  off 
the  transverse  portion  of  the  arch,  the  radial  and  carotid  pulses  on  one 
side  may  differ  from  those  on  the  opposite  side. 

If,  for  instance,  the  innominate  artery  is  compressed  or  its  opening 
is  partially  blocked  by  clot,  the  right  radial  pulse  will  be  smaller  than  the 
left.  In  the  same  way  the  opening  of  the  left  subclavian  may  be  involved, 
thus  giving  rise  to  a  smaller  pulse  in  the  left  radial. 

If,  on  the  other  hand,  the  sac  is  interposed  between  the  innominate 


748 


DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


artery  and  the  left  subclavian  and  carotid  arteries,  there  will  be  a  delay 
in  the  appearance  of  the  left  pulse.  The  carotid  pulse  will  often  show  the 
same  changes.  It  is  thus  seen  that  inequality  or  retardation  of  the 
pulse  is  a  valuable  sign.  Simultaneous  tracings  of  the  two  radials  will 
often  show  the  most  marked  differences  in  cases  of  aneurism.  Inequality 
of  the  radial  pulses  alone  can  occur  in  conditions  other  than  aneurism, 
such,  for  instance,  as  an  anomalous  radial  artery  on  one  side,  the  pressure 
of  a  tumor  on  the  subclavian  or  axillary  artery,  or  blocking  of  the  orifice 
of  the  innominate  or  left  subclavian  artery  in  cases  of  extensive  athero- 
matous disease  of  the  aorta. 

Percussion. — Unless    the    aneurism    is    very    small    or    deep-seated, 
dulness  on  percussion  can  be  elicited  over  that  portion  of  the  chest  wall 


Fig.  409. — Aortic  aneurism  (syphilitic)  in  mulatto,  aged  62.     Shortness  of  breath  on  exer- 
tion; chest  pain.      Physical  signs  of  aortic  and  mitral  insufficiency. 


which  overlies  the  arch.  The  areas  over  which  dulness  is  most  commonly 
encountered  correspond  to  those  in  which  pulsation  is  noted,  namely, 
the  second  and  third  interspaces  just  to  the  right  and  to  the  left  of  the  ster- 
num and  over  the  manubrium.  Dulness  over  the  dorsal  vertebra?  may 
be  present,  even  early  in  the  disease. 

There  may  be  a  small  area  of  marked  dulness  at  one  of  these  points 
and  beyond  an  area  of  relative  dulness.  In  cases  of  dilatation  of  the 
aorta,  dulness  may  extend  across  the  sternum  and  for  some  distance  on  either 
side,  at  the  level  of  the  second  and  third  interspaces  (Fig.  409).  If  a 
tumor  is  present,  the  size  of  the  sac  may  be  determined,  approximately,  by 
the  area  of  relative  dulness  which  extends  around  the  tumor.     In  cases 


ANEURISM    OF    THE    THORACIC    AORTA  749 

of  aneurism  of  the  descending  thoracic  aorta,  dulness  may  be  detected  in 
the  left  interscapular  region  or  about  the  angle  of  the  left  scapula.  The 
occurrence  of  localized  pain  and  dulness  oyer  the  painful  area  is  suggestive 
of  aneurism  even  if  other  symptoms  and  signs  are  absent.  Occasionally 
percussion  over  the  upper  part  of  the. sternum  is  accompanied  by  pain 
or  a  severe  paroxysm  of  coughing  when  there  is  no  other  evidence  of 
aneurism  (Eichhorst). 

Percussion  of  the  cardiac  area  will  often  show  no  enlargement  of  the 
heart,  although  it  may  be  displaced  downwards  and  to  the  left  by  the 
aneurismal  sac.  Hypertrophy  is  most  apt  to  occur  if  the  patient  is  also 
the  victim  of  a  general  arterio-sclerosis,  Bright 's  disease  or  aortic  re- 
gurgitation. 

Auscultation. — The  auscultatory  signs  in  aneurism  are  not  distinctive 
and  are  relatively  of  less  importance  than  the  signs  elicited  by  the  other 
procedures.  Very  often  the  heart  sounds  are  as  distinctly  heard  over 
the  aneurism  as  over  the  body  of  the  heart  itself,  giving  the  impression 
of  there  being  a  second  heart.  A  murmur,  usually  systolic  in  time, 
is  often  heard ;  the  murmur  may  be  diastolic  in  time,  especially  if  the  first 
portion  of  the  arch  is  involved  or  there  may  be  a  to-and-fro  murmur. 
Probably  the  most  distinctive  auscultatory  sign  is  the  presence  of  a  ring- 
ing and  sharply  accentuated  second  aortic  sound.  The  farther  this 
accentuated  second  sound  is  heard  from  the  aortic  cartilage,  the  more 
significant  it  becomes.  Even  with  the  presence  of  a  diastolic  murmur 
the  second  sound  is  rarely  entirely  replaced.  If  the  unaided  ear  or  a 
rigid  stethoscope  is  used,  the  diastolic  shock  may  be  felt  coincidently 
with  the  hearing  of  the  accentuated  second  sound. 

The  heart  itself  may  show  no  abnormality.  In  the  terminal  stages, 
however,  there  may  be  the  evidences  of  failing  compensation. 

Pressure  on  the  trachea  may  cause  a  weak  and  feeble  respiratory 
murmur  over  both  lungs.  If  the  pressure  is  exerted  on  one  of  the  main 
bronchi,  usually  the  left,  the  respiratory  murmur  on  the  corresponding- 
side  may  be  less  tense  than  over  the  opposite  lung.  Complete  occlusion 
of  a  main  bronchus  will  cause  an  entire  absence  of  breath  sounds  over 
the  affected  lung. 

Blood-pressure. — If  there  is  present  a  widespread  arterio-sclerosis 
or  Bright 's  disease  marked  arterial  hypertension  may  occur  but  in  the 
majority  of  cases  of  thoracic  aneurism  the  blood-pressure  is  normal. 
If,  however,  the  pressure  is  taken  in  both  arms  there  may  be  quite  a 
marked  difference  in  the  two  sides;  this  has  the  same  significance  as 
inequality  or  retardation  of  the  pulse  wave,  as  determined  by  the  pal- 
pating finger.  Pressure  differences  of  5  mm.  are  common  in  arterio- 
sclerotic subjects  without  aneurism.  In  the  latter  condition  unilateral 
differences  of  10  to  20  mm.  are  not  rare. 

X-ray  Examination. — So  thoroughly  have  the  X-rays  demonstrated 
their  usefulness  in  mediastinal  affections  that  no  examination  in  case 
of  a  suspected  aneurism  can  be  considered  as  being  complete  without 
their  employment.  Even  in  cases  in  which  the  physical  signs  and  symp- 
toms leave  little  room  for  doubt,  the  X-rays  enable  us  to  determine  the 
extent  and  the  character  of  the  aneurism  and  whether  there  is  more 
than  one  portion  of  the  aorta  which  is  involved.  The  existence  of  not 
a  few  aneurisms  is  first  revealed  as  the  result  of  a  fluoroscopic  or  radio- 
scopic  examination  which  has  been  made  for  some  other  purpose. 


750  DISEASES    OF   THE   PERICARDIUM,    HEART,    AND    AORTA 

Classification     of     Aneurisms    Involving    the    Thoracic    Aorta. —  1. 

Aneurism  of  the  Intrapericardial  Portion  of  the  Arch  and  Sinuses  of 
Valsalva.- — When  the  thoracic  aorta  is  involved,  the  aneurism  most  fre- 
quently occurs  in  the  ascending  portion  of  the  arch.  This  is  due  to  the 
fact  that  a  syphilitic  mesaortitis  is  so  commonly  limited  to  the  first  portion 
of  the  vessel.  It  may  involve  one  or  all  of  the  sinuses  of  Valsalva.  In 
this  situation  the  aneurism  is  usually  small,  and  deeply  placed;  it  is 
frequently  first  discovered  at  the  autopsy  table  or  as  the  result  of  an  X-ray 
examination  (see  Fig.  404).  During  life  the  clinical  picture  is  apt  to  be 
that  of  angina  pectoris  or  aortic  insufficiency.  This  is  due  to  the  fact 
that  the  exciting  cause  of  the  aortitis  may  lead  to  a  partial  occlusion  of  the 
orifices  of  the  coronary  arteries  or  it  may  produce  aortic  incompetence, 
either  by  dilating  the  aortic  ring  or  by  extension  of  the  disease  to  the  valve 
leaflets.     In  the  presence  of  either  one  of  these  conditions,  therefore,  an 


Fig.  410. — Large  aneurismal  tumor  presenting  to  the  left  of  the  sternum. 

aneurism  should  be  suspected.  An  aneurism  in  this  situation  may  com- 
press the  superior  vena  cava  and  thus  cause  congestion  of  the  face  or 
undue  fulness  of  the  jugulars  and  the  veins  of  one  or  other  upper 
extremity. 

2.  Aneurism  of  Ascending  Arch. — This  includes  that  portion  of  the 
aorta  between  the  sinuses  of  Valsalva  and  the  orifice  of  the  innominate 
artery.  An  aneurism  in  this  situation  commonly  attains  a  very  large  size 
and  this  may  occur  without  symptoms,  or  the  symptoms  may  be  very 
trivial  in  nature.  For  this  reason  an  aneurism  affecting  this  portion  of  the 
aorta  has  been  called  the  aneurism  of  physical  signs.  The  heart  is  often 
dislocated  downward.  The  aneurismal  tumor  extends  upward  and  to 
the  right  appearing  in  the  second  and  third  interspaces  to  the  right  of  the 
sternum  (see  Fig.  399) ;  it  may,  however,  appear  to  the  left  of  the  sternum 
(Fig.  410).  Varying  degrees  of  pain  may  occur,  especially  when  the  ribs 
and  sternum  are  being  eroded.     Dyspnea,  substernal  oppression  or  pain 


ANEURISM  OF  THE  THORACIC  AORTA  751 

are  apt  to  be  increased  by  exertion.  Pressure  symptoms  are  relatively 
infrequent  in  this  situation  but  compression  of  the  superior  cava  may 
occur  as  shown  by  distention  of  the  veins  and  congestion  of  the  head, 
neck  and  upper  extremities.  Rarely  the  inferior  vena  cava  may  be 
compressed,  giving  rise  to  edema  of  the  feet  and  legs. 

3.  Aneurism  of  the  Transverse  Portion  of  the  Arch. — This  is  the 
aneurism  of  symptoms.  The  transverse  portion  of  the  aorta  is  not  only 
firmly  fixed  but  is  in  close  relations  with  several  important  structures. 
Behind  it  lie  the  trachea,  esophagus  and  thoracic  duct ;  below  is  the  left 
bronchus;  and  curving  around  it  is  the  left  recurrent  laryngeal  nerve. 
Being  deeply  placed  an  aneurism  may  develop  in  the  transverse  arch 
without  giving  any  physical  signs.  On  the  other  hand,  pressure  symp- 
toms are  usually  marked  as  the  close  relation  of  various  important  struc- 
tures renders  them  liable  to  compression  even  by  a  relatively  small 
aneurism.  The  aneurismal  tumor  may  extend  in  any  direction  but 
usually  it  grows  backward;  it  may,  however,  project  forward  presenting 
a  little  to  the  right  and  left  of  the  median  line. 

In  aneurisms  of  the  ascending  portion  of  the  arch  the  pulses  are  equal 
as  the  sac  is  located  on  the  proximal  side  of  the  innominate  and  left  carotid 
and  subclavian  arteries.  When  the  transverse  arch  is  the  seat  of  the 
aneurism,  either  the  orifices  of  the  main  bronchus  may  be  included  in  the 
sac  or  the  bulging  may  take  place  between  the  innominate  artery  and  the 
left  carotid  and  subclavian  arteries.  In  either  case  an  inequality  of  the 
pulse  waves  is  produced  in  the  two  radial  and  carotid  arteries.  An 
aneurism  in  this  situation  does  not,  as  a  rule,  attain  a  very  great  size  and 
a  fatal  termination  is  apt  to  occur  at  a  much  earlier  period  than  in  the 
case  of  aneurisms  of  the  ascending  portions  of  the  arch. 

Pulsation  may  be  absent  but  often  the  presence  of  a  slight  impulse  can 
be  detected  by  making  firm  pressure  over  the  manubrium  with  the  palm  of 
the  hand.  Dulness  may  be  noted  in  the  same  situation.  An  aortic 
systolic  murmur  and  an  accentuated  second  sound  are  frequently  heard. 

Pressure  symptoms  are  common  and  may  be  the  only  evidence  of  an 
aneurism.  Thus  there  may  be  pain  o-r  difficulty  in  swallowing;  dyspnea, 
which  may  be  paroxysmal  in  character;  hoarseness;  a  brassy  cough;  and 
hemoptysis. 

Not  infrequently  the  ascending  and  transverse  portions  of  the  arch 
are  involved  together. 

4.  Descending  Portion  of  the  Arch. — This  portion  of  the  aorta  lies  to  the 
left  side  of  the  dorsal  vertebra  from  the  third  to  the  sixth.  The  only 
important  structures  near  it  are  the  esophagus  and  left  bronchus.  An 
aneurism  in  this  situation  usually  grows  backward  and  erodes  the  verte- 
bra or  it  may  compress  the  esophagus  and  rupture  into  it  (see  Fig.  410). 
There  is  a  paucity  of  both  symptoms  and  physical  signs  in  an  aneurism 
in  this  location.  If  one  has  reason  to  suspect  a  thoracic  aneurism  the  left 
interscapular  region  and  the  area  about  the  angle  of  the  left  scapula 
should  be  carefully  examined  as  a  tumor  sometimes  appears  in  these 
locations. 

Commonly  pain  is  the  only  manifestation.  This  may  be  of  a  dull 
aching  character  or  a  sharp,  shooting  neuralgic  pain.  The  pain  may  be 
localized  at  one  point  along  the  vertebral  column  or  it  may  radiate  around 
the  body  and  down  the  left  arm  and  is  often  intense.  The  condition  is 
often  mistaken  for  Potts'  disease.     Musser  states  that  an  aneurism  in  this 


752  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

situation  often  simulates  phthisis  very  closely.  The  fact  that  tuberculosis 
is  not. uncommon  in  those  subject  to  aneurism  of  the  aorta  often  masks 
the  presence  of  the  latter. 

5.  Descending  Thoracic  Aorta. — This  portion  of  the  aorta  extends 
from  the  sixth  to  the  twelfth  dorsal  vertebra  where  it  becomes  continuous 
with  the  abdominal  aorta.  An  aneurism  in  this  portion  of  the  aorta  is 
not  common  and  when  present  it  usually  occurs  near  the  diaphragmatic 
opening.  The  aneurismal  tumor  usually  extends  backward  and  often 
erodes  the  vertebra.  It  may,  however,  project  forward  and  if  located 
just  above  the  diaphragmatic  opening  cause  epigastric  pulsation. 

Dysphagia  sometimes  occurs  but,  as  a  rule,  the  only  symptom  is  pain. 
This  varies  greatly.  It  may  be  very  slight  or  it  may  be  persistent  and  of 
the  most  excruciating  character. 

Diagnosis. — In  the  majority  of  cases  the  first  evidence  of  trouble  is 
a  sense  of  substernal  oppression  or  actual  pain  especially  after  exertion. 
If  there  are  associated  with  the  pain  pressure  symptoms  or  physical  signs, 
the  existence  of  an  aneurism  is  always  to  be  thought  of.  The  symptoms 
and  the  location  and  nature  of  the  physical  signs  have  been  fully  dealt 
with  and  need  not  be  discussed  here. 

The  three  conditions  which  are  most  apt  to  be  confused  with  aneurism 
are:  (1)  a  mediastinal  tumor;  (2)  pulmonary  tuberculosis;  and  (3)  mitral 
stenosis. 

While  a  mediastinal  tumor  bordering  the  vertical  axis  of  the  chest  may 
give  rise  to  signs  they  are  more  apt  to  occur  in  or  extend  to  areas  not  in- 
volved by  a  thoracic  aneurism.  The  tumor,  as  a  rule,  does  not  perforate 
the  chest  wall  nor  is  it  associated  with  expansile  pulsation,  a  ringing 
second  aortic  sound  or  diastolic  shock.  The  presence  of  arterio-sclerosis 
and  a  positive  Wassermann  reaction  are  points  in  favor  of  the  trouble 
being  an  aneurism. 

At  first  sight  there  seems  no  good  reason  why  phthisis  and  aneurism 
should  be  confused.  When  we  recall,  however,  that  dyspnea,  hoarseness, 
chest  pain,  cough,  hemoptysis  and  loss  of  weight  are  common  in  both  and 
that  dulness  may  extend  upward  toward  the  apex  of  the  lung  or  unilat- 
eral suppression  of  the  breath  sounds  may  occur  in  aneurism,  one  can 
understand  how  mistakes  occur.  In  aneurism  there  is  either  no  fever  or  it 
is  very  slight.  In  addition  physical  signs  of  vascular  disease  are  usually 
present  in  aneurism  and  the  sputum  does  not  contain  tubercle  bacilli. 
It  must  not  be  forgotten,  however,  that  the  two  conditions  are  not  un- 
commonly associated. 

Although  paralysis  of  the  left  vocal  cord  as  the  result  of  pressure  on  the 
recurrent  laryngeal  nerve  in  cases  of  mitral  stenosis  is  not  common,  it  must 
be  kept  in  mind  as  the  paralysis,  hoarseness  and  a  brassy  cough  have  led  to 
a  diagnosis  of  aneurism.  Careful  auscultation  of  the  heart  will  usually 
prevent  such  a  mistake. 

Special  Forms  of  Aneurism 

dilatation  of  the  aorta 

By  many,  simple  passive  dilatation  of  the  aorta  is  not  considered  as 
being  a  true  aneurism.  If,  however,  we  embrace  under  the  term  "aneu- 
rism" cases  in  which  the  lumen  of  the  arterial  tube  is  uniformly  expanded, 
simple  dilatation  must  be  included.     The  condition  really  represents  an 


ANEURISM    OF    THE    THORACIC    AORTA  753 

incipient  form  of  aneurism  and  while  it  lacks  some  of  the  features  of  the 
saccular  variety,  it  has  many  symptoms  and  physical  signs  in  common 
with  that  type  of  the  disease. 

Etiology. — There  are  two  forms  of  dilatation  of  the  aorta,  namely, 
passive  and  dynamic.  The  former  is  due  to  a  gradual  increase  in  the 
diameter  of  a  portion  of  the  aorta  or  even  the  entire  arch,  the  lumen  of  the 
vessel  remaining  permanently  stretched.  In  the  dynamic  form  the  aorta 
may,  as  the  result  of  a  powerfully  acting  heart,  become  abnormally  large 
during  each  systole  but  during  the  diastolic  period  retract  to  its  normal 
size. 

Passive  dilatation  of  the  aorta  is  most  frequently  encountered  in 
association  with  arterio-sclerosis,  especially  in  old  people  in  whom 
atheromatous  changes  are  marked.  The  next  most  common  cause  is 
aortic  insufficiency  which  in  many  cases  is  associated  with  syphilitic 
aortitis.  Negroes  furnish  many  examples  of  dilatation  of  the  aorta  due 
to  the  fact  that,  as  a  race,  they  are  extremely  prone  to  develop  degenera- 
tive changes  in  the  arteries  as  the  result  of  a  syphilitic  infection.  In 
McCrea's  series  of  35  cases  no  less  than  14  were  negroes. 

From  X-ray  studies  Smith  and  Kilgore1  determined  that  the  diameter 
of  the  aorta  might  be  increased,  in  extreme  instances,  to  nearly  twice  its 
normal  size  as  the  result  of:  (1)  syphilitic  aortitis;  (2)  arterio-sclerosis,  in 
individuals  over  fifty  years  of  age;  (3)  chronic  endocarditis,  especially 
in  the  relatively  young;   and  (4)  arterial  hypertension. 

Among  the  more  infrequent  etiological  factors  may  be  mentioned  the 
acute  infectious  diseases,  especially  acute  rheumatic  fever,  anemia  and 
Graves'  disease. 

Morbid  Anatomy. — The  primary  cause  in  nearly  all  cases  is  a  diseased 
aorta,  the  dilatation  being  a  secondary  manifestation.  The  aorta  may 
dilate  at  any  point  but  the  most  frequent  site  is  the  ascending  portion  of 
the  arch  which  is  also  most  subject  to  atheromatous  and  syphilitic  disease 
(Fig.  411). 

Passive  stretching  of  the  aorta  may  be  caused,  occasionally,  as  the 
result  of  a  blood-pressure  which  persistently  remains  high.  In  such 
instances  the  intima  may  be  smooth  or  show  but  little  evidence  of  an 
endarteritis  deformans. 

The  dilatation  may  be  cylindrical  or  fusiform  in  shape.  In  some 
instances  the  great  vessels  given  off  from  the  arch  are  also  involved. 

When  the  first  portion  of  the  aorta  becomes  dilated,  the  aortic  ring- 
may  also  be  involved  thus  giving  rise  to  aortic  insufficiency  and  cardiac 
hypertrophy.  This  is  especially  apt  to  occur  when  the  aortic  lesion  is 
syphilitic  in  origin.  Other  organic  heart  lesions,  either  valvular  or 
muscular,  are  common. 

Symptoms. — Dilatation  of  the  aorta  may  be  present  without  any 
symptoms,  or  the  symptoms  may  be  so  trivial  as  not  to  attract  attention. 
In  the  latent  form  the  condition  is  usually  an  accidental  discovery  in  the 
post-mortem  room.  Now  that  the  X-rays  are  being  used  so  generally 
for  diagnostic  purposes  many  examples  of  a  dilated  aorta  are  coming  to 
light  which  otherwise  would  have  been  unsuspected.  Furthermore,  the 
more  exact  knowledge  which  now  prevails  as  to  the  etiology  of  aortic 
valvular  lesions  is  directing  more  attention  to  the  aorta. 

In  addition  to  the  latent  form  there  are  two  fairly  definite  types:  (1) 
1  Am.  Jour.  Med.  Sc,  April,  1915. 


754 


DISEASES    OF    THE    PERICARDIUM,    HEART,    AXD    AORTA 


That  in  which  the  clinical  picture  is  that  of  angina  pectoris  and  (2)  that 
in  which  the  principal  features  are  those  of  organic  heart  disease,  usually 
aortic  insufficiency. 

In  the  anginal  type,  especially  in  the  senile  form  of  dilatation,  attacks 
of  true  angina  may  recur  for  several  years.  Instead  of  pain  there  may  be 
a  sense  of  substernal  oppression,  especially  after  exertion. 

In  the  cardiac  form  there  may  be  attacks  of  faintness;  shortness  of 
breath  on  exertion,  cough,  and,  finally,  all  the  symptoms  of  broken  com- 


Fig.   411. — Showing  dilatation  of  the  aorta  with  slight  bulging  to  the  right. 

pensation.  The  most  frequent  cardiac  lesion  is  aortic  insufficiency,  the 
leakage  being  clue  in  some  instances  to  disease  of  the  aortic  leaflets,  in 
others  to  stretching  of  the  aortic  ring. 

Physical  Signs. — Inspection.- — In  old  people  with  rigid  chest  walls 
there  may  be  no  visible  impulse.  When  present,  the  impulse  may  be 
most  noticeable  in  the  suprasternal  notch;  it  also  may  be  noted  in  the 
second  and  third  interspaces  to  the  right  of  the  sternum  or  over  the  manu- 
brium.    When  the  aorta  becomes  dilated  the  main  branches  are  some- 


ANEURISM  OF  THE  THORACIC  AORTA 


755 


times  lifted  upward  so  that  pulsation  in  the  right  subclavian  is  seen  above 
instead  of  below  the  clavicle. 

Palpation. — In  the  absence  of  visible  pulsation  the  impulse  may  be  felt 
by  pushing  a  finger  downwards  in  the  suprasternal  notch  or  by  applying 
the  palm  of  the  hand  firmly  over  the  manubrium.  A  systolic  thrill  local- 
ized over  the  aortic  area  and  a  diastolic  shock  in  the  same  region  are  not 
infrequent.  If  aortic  insufficiency  is  present,  there  may  be  a  diastolic  thrill. 
Except  in  those  cases  in  which  dilatation  has  been  produced  by  arterial 
hypertension  the  blood-pressure  is,  as  a  rule,  low. 


Pulsating  carotids 


Pulsating  jugulars 


Apex  impulse  displaced 
wnward  and  outward 


Fig.  412. 


-Physical  signs  in  aortic  insufficiency  due  to  dilatation  of  the  aorta, 
indicate  the  diastolic  murmur. 


The  dots 


Percussion. — Dulness  over  the  manubrium  above  the  level  of  the 
second  ribs  may  be  caused  by  extension  of  the  aorta  upward;  this  is  the 
most  constant  single  sign  (Osier).  Lateral  expansion  of  the  artery  may 
be  indicated  by  dulness  in  the  second  and  third  interspaces  to  the  right  or 
left  of  the  sternum.  Owing  to  the  frequent  association  of  aortic  insuffi- 
ciency with  dilatation  of  the  aorta  the  area  of  cardiac. dulness  is  often 
greatly  increased  (Fig.  412). 

Auscultation. — A  systolic  murmur  having  its  punctum  maximum  at 
the  aortic  cartilage  and  transmitted  to  the  carotids,  is  often  heard.  This 
murmur  is  generated  in  the  dilated  portion  of  the  aorta  as  the  result  of  the 
blood  being  thrown  into  swirls.  Projecting  calcareous  plates  majr  also  aid 
in  producing  the  murmur.  The  second  sound  is  sharply  accentuated  and 
ringing  or  clanging  in  character.  This  serves  to  distinguish  the  systolic 
murmur  from  that  occurring  in  aortic  stenosis  in  which  the  second  sound 
is  very  faint  or  not  heard  at  all.  If  aortic  insufficiency  is  present,  there  is 
also  a  diastolic  murmur  which  may  occur  alone  or  in  association  with  the 


756  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 

systolic  bruit.  In  aortic  insufficiency  due  to  stretching  of  the  aortic  ring, 
the  diastolic  murmur  rarely  replaces  entirely  the  ringing  second  sound  as 
is  apt  to  be  the  case  when  the  leakage  has  been  caused  by  acute  endocar- 
ditis. Another  point  of  difference  is  that  the  diastolic  murmur  occurring 
with  dilatation  of  the  aorta  is  often  transmitted  upward. 

ARTERIO-VENOUS  ANEURISM 

Communication  between  an  artery  and  vein  is  not  an  infrequent 
occurrence  in  the  peripheral  vessels  and  is  usually  the  result  of  a  trauma. 
Gunshot  wounds,  especially  those  produced  by  the  modern  type  of 
bullet,  are  the  most  common  causes  of  this  accident. 

Involvement  of  the  large  vessels  in  the  thorax  is  relatively  rare. 
The  aneurism  may  perforate  the  superior  vena  cava,  one  of  the  pulmonary 
arteries  or  one  of  the  auricles. 

Superior  Vena  Cava.- — An  aneurism  of  the  ascending  portion  of  the 
arch  sometimes  ruptures  into  the  vena  cava.  As  a  rule,  death  occurs 
in  a  few  hours  but  the  patient  may  survive  for  months. 

When  the  perforation  occurs,  the  patient  is  suddenly  seized  with 
intense  dyspnea,  the  face  becomes  cyanosed  and  the  veins  in  the  neck 
greatly  distended.  In  the  course  of  a  few  hours  a  tense  edema  of  the  face 
and  neck  appears.  Later  the  veins  over  the  chest  become  enlarged  from 
collateral  circulation  established  between  the  internal  mammary,  the 
intercostals  and  the  epigastric  veins.  The  enlargement  of  the  veins 
terminates  abruptly  at  the  level  of  the  diaphragm.  Over  the  site  of 
the  perforation,  in  the  area  about  the  aortic  cartilage,  there  may  be 
a  marked  thrill.  In  addition  there  is  a  continuous,  roaring  murmur  with 
systolic  intensification. 

According  to  Osier  the  only  other  condition  which  gives  rise  to 
sudden  cyanosis  of  the  head  and  neck  is  a  severe,  crushing  accident  to  the 
thorax. 

Pulmonary  Artery. — Perforation  into  the  pulmonary  artery  is  at- 
tended with  sudden  and  severe  dyspnea  followed  by  cough  and  occasionally 
with  blood-streaked  sputum.  A  thrill  over  the  pulmonic  area  is  occa- 
sionally present.  The  most  characteristic  physical  sign  is  a  continuous, 
roaring  murmur,  with  a  systolic  intensification  heard  over  the  pulmonic 
area.  Perforation  of  the  pulmonary  artery  is  not,  as  a  rule,  immedi- 
ately fatal.  A  period  of  weeks  or  even  months  may  elapse  before  death 
occurs. 

Auricles  of  the  Heart. — Death  usually  occurs  within  a  few  minutes. 
There  may  be  dyspnea,  cough  and  cyanosis,  but  in  most  of  the  reported 
cases  there  have  been  no  characteristic  symptoms. 

ANEURISM  OF  THE  INNOMINATE  ARTERY 

When  the  transverse  portion  of  the  arch  is  implicated,  the  first  part 
of  the  innominate  is  frequently  included  in  the  aneurismal  sac.  When 
such  is  the  case,  the  only  clinical  manifestation  of  involvement  of  the 
innominate  is  a  diminution  or  retardation  of  the  pulse  wave  on  the 
right  side.  The  innominate  may  be  involved  either  independently  of, 
or  in  association  with  an  aneurism  of  the  aorta. 

The  principal  symptoms  occurring  in  an  aneurism  of  the  innominate 


ANEURISM    OF   THE    THORACIC    AORTA  757 

artery  are  dyspnea,  pain  and  a  throbbing  sensation  at  the  root  of  the 
neck.     Dysphagia  may  also  occur. 

As  a  rule,  the  aneurismal  sac  presents  behind  or  just  above  and  to 
the  right  of  the  right  sterno-clavicular  joint.  The  sac  usually  extends 
forward  and  not  infrequently  causes  a  dislocation  of  the  right  sterno- 
clavicular joint.  The  right  radial  pulse  is  retarded  or  less  full  than  the 
left.  The  right  external  jugular  is  commonly  distended  and  there  may 
be  edema  of  the  right  side  of  the  face  and  neck.  On  palpation  there  is  a 
thrill  and  in  common  with  other  aneurisms,  the  pulsation  is  felt  to  be 
expansile  in  character.  A  diastolic  shock  is  also  felt.  As  the  innomi- 
nate crosses  in  front  of  the  trachea  the  sac  may  become  attached  to  it 
and  give  rise  to  a  tracheal  tug. 

On  auscultation  there  may  be  a  systolic  murmur.  Pressure  on  the 
lung  often  causes  an  impairment  of  the  percussion  note  and  feeble  breath 
sounds  at  the  right  apex. 

An  aneurism  of  the  innominate  is  to  be  distinguished  from  aneurism  of 
the  arch  by  reason  of  the  fact  that  the  latter  rarely  extends  as  high  as 
the  clavicle.  If  an  aneurism  occurs  in  both  situations,  the  one  in  the 
innominate  may  be  overlooked  unless  the  tumor  is  plainly  visible. 

In  both  dynamic  and  passive  dilatation  of  the  arch  of  the  aorta  the 
subclavian  is  not  infrequently  lifted  up  so  that  there  is  a  marked  pulsa- 
tion just  above  and  to  the  right  of  the  sterno-clavicular  joint.  This  is 
sometimes  referred  to  as  a  phantom  aneurism.  Furthermore,  a  rela- 
tively frequent  finding  is  the  presence  of  a  systolic  murmur  in  the  sub- 
clavian arteries.  It  is  practically  always  functional  in  character  and  is 
thought  to  have  some  connection  with  an  apical  tuberculosis.  These 
facts  must  be  kept  in  mind  when  considering  the  possibility  of  aneurism. 
In  those  instances  in  which  the  subclavian  artery  is  lifted  up  as  the 
result  of  dilatation  of  the  aorta  there  is  no  difference  in  the  two  radial 
pulses. 

RUPTURE  OF  THE  AORTA 

Etiology. — Rupture  of  one  of  the  coats  of  the  aorta  may  occur  in  a 
healthy  vessel  as  the  result  of  a  fall  or  a  severe  blow  on  the  chest.  The 
occurrence  of  such  an  accident  is  rare.  Although  cases  have  been  reported 
in  which  rupture  of  a  healthy  aorta  is  said  to  have  followed  unusual 
muscular  effort,  the  weight  of  authority  is  against  the  probability  of  such 
an  accident.  It  is  more  than  likely  that  in  all  such  cases  there  has  been 
some  degeneration  of  the  aorta. 

In  the  vast  majority  of  cases  of  rupture  of  the  aorta  the  vessel  has  be- 
come the  seat  of  atheromatous  or  syphilitic  disease.  When  this  occurs, 
any  unusual  muscular  strain  may  cause  the  intima  to  split.  In  some  in- 
stances the  intima  may  be  torn  while  the  patient  is  at  rest :  in  such  cases 
an  abnormally  high  blood-pressure  may  be  the  exciting  cause. 

Morbid  Anatomy. — I  have  already  emphasized  the  fact  that  the  pri- 
mary lesion  in  degenerative  diseases  of  the  blood-vessels  occurs  in  the 
media  and  that  for  some  time  the  intima  may  present  a  normal  appear- 
ance. The  lesion  in  the  media,  however,  constitutes  a  point  of  weakened 
resistance  and  any  abnormal  strain  within  the  vessel  may  cause  the  over- 
lying intima  to  split.  In  the  most  severe  forms  of  rupture  all  three  coats 
may  be  torn  at  once  with  an  immediately  fatal  result.     But  in  the  ma- 


758  DISEASES    OF    THE    PERICARDIUM,    HEART,    AND    AORTA 


Fig.  413. — Rupture  of  the  aorta.  Clinical  Notes:  Sudden  death  without  premoni- 
tory symptoms  during  convalescence,  six  days  after  an  operation  for  hemorrhoids. 
Pathologic  Notes:  Two  and  one-half  centimeters  above  the  attachment  of  the  aortic 
valves  there  is  a  rough,  slightly  shaggy  looking  tear  running  directly  across  the  aorta.  It  is 
2  cm.  in  length  and  leads  directly  from  a  small  aneurismal  pouch  into  the"pericardial  cavity. 
The  surface  of  the  aorta  along  the  ascending  arch  shows  small,  scattered,  yellowish  nodules. 
(Specimen  from  the  Pennsylvania  Hospital.     Pathologist:  Dr.  G.  C.  Robinson.) 


ANEURISM    OF    THE    THORACIC    AORTA  759 

jority  of  cases  the  intima  is  first  torn.  "When  this  occurs  several  things 
may  happen:  (1)  Complete  rupture  of  the  vessel  may  succeed  the  tearing 
of  the  intima.  This  may  occur  in  a  few  hours  or  it  may  be  delayed  for  a 
number  of  days.  (2)  Instead  of  the  remaining  coats  being  torn  the  vessel 
begins  to  bulge  at  the  point  of  injur}-  and  a  saccular  aneurism  is  formed. 
This  is  probably  the  most  frequent  termination  of  a  tear  in  the  intima. 
(3)  The  blood  may  burrow  between  the  intima  and  media  or  between  the 
media  and  adventitia  and  form  what  is  known  as  a  dissecting  aneurism.. 
In  such  cases  death  may  occur  at  once ;  or  the  blood  may  break  through 
the  media  and  intima  at  a  lower  point  and  again  communicate  with  the 
lumen  of  the  vessel;  or  external  rupture  may  occur  at  some  future  time. 
A  few  cases  have  been  recorded  in  which  the  dissecting  aneurism  healed. 

The  most  frequent  site  of  the  rupture  is  in  the  first  or  ascending  portion 
of  the  aorta  (Fig.  413).  There  are  two  reasons  for  this:  (1)  the  greater 
frequency  of  syphilitic  and  atheromatous  disease  in  this  situation ;  and  (2) 
the  blood,  as  it  is  forcibly  expelled  from  the  ventricle  at  each  systole, 
rapidly  expands  the  aorta.  If,  therefore,  the  vessel  wall  is  weakened  by 
disease,  a  rupture  of  the  intima  may  readily  occur  and  especially  after 
unusual  effort.  The  tear  in  the  intima  may  be  transverse  or  vertical  and 
is  usually  clean  cut. 

Symptoms. — In  many  cases  death  is  instantaneous  and  the  true  nature 
of  the  trouble  is  first  revealed  at  the  autopsy  table. 

In  those  instances  in  which  death  does  not  occur  immediately,  pain 
is  the  most  prominent  symptom.  This  may  be  substernal  and  of  moder- 
ate severity.  It  is  not  infrequent  in  the  early  stages  of  aneurism,  probably 
as  the  result  of  tearing  the  intima.     Later  this  pain  disappears. 

In  those  cases  in  which  external  rupture  takes  place  the  initial  tear 
in  the  intima  and  media  is  attended  by  severe  substernal  pain  and  the 
signs  of  collapse.  Death  may  occur  at  once.  Not  infrequently,  how- 
ever, there  is  an  interval  which  may  last  from  a  few  hours  to  two  weeks, 
when  the  patient  is  again  seized  with  pain  and  almost  immediately  expires. 


INDEX 


Abortive  pneumonia,  409 
Abscess,  diaphragmatic,  596 

of  lung,  bronchiectasis  and,  285 
of  myocardium,  627 
pulmonary,  458 

bronchiectasis  and,  464 
mortality  from,  464 
multiple,  diagnosis,  465 
etiology,  464 
morbid  anatomy,  465 
physical  signs,  465 
symptoms,  465 
single,  458 
diagnosis,  464 
etiology,  458 
morbid  anatomy,  458 
physical  signs,  463 
sputum  in,  463 
symptoms,  462 
termination,  460 
tuberculosis  and,  464 
subphrenic,  596 
Acidosis  in  myocarditis,  632 
Acoustics  in  physical  diagnosis,  53 
of  heart  murmurs,  220 
sounds,  212 
Acromegaly,      pulmonary     osteo-arthro- 

pathy  and,  526 
Actinomycosis,  pulmonary,  diagnosis,  383 
etiology,  381 
morbid  anatomy,  382 
physical  signs,  383 
Adams-Stokes  syndrome,  632,  637 
Adenoids  and  enlarged  thymus,  513 
Adhesive  pericarditis,  610,  623 

Flint's  murmur  in,  675 
Age  in  percussion  of  lungs,  101 

influence  of,  in  tuberculosis,  299 
Air  emboli,  471 

Alcoholic  subjects,  pneumonia  in,  409 
Allorhythmia,  169 
Amphoric  breathing,  119 
Anaphylaxis,  asthma  and,  272 
Anasarca,  cardiac,  244 
Anatomy  of  diaphragm,  576 


Anemia  in  chronic  infectious  endocardi- 
tis, 653 
in  tuberculosis,  324 
murmurs  in,  240 
Aneurism,  arterio-venous,  731,  756 
false,  731 

infective  emboli  and,  733 
mitral  stenosis  and,  676 
mycotic,  733 
of  aorta,  731 

ascending  arch,  750 

blood  pressure  in,  749 

brassy  cough  in,  741 

bronchi  and,  742 

classification,  750 

diagnosis,  752 

diastolic  shock  in,  746 

dissecting,  731 

esophagus  and,  741 

etiology,  732 

hemoptysis  in,  743 

intrapericardial,  750 

laryngeal  nerve  in,  741 

lungs  in,  742 

mediastinal  tumor  and,  752 

mitral  stenosis  and,  752 

morbid  anatomy,  733 

pain  in,  740 

peripheral  arteries  in,  747 

phrenic  nerve  in,  741 

physical  signs,  744 

pressure  effects,  740 

pulsation,  747 
simulating,  745 

rupture,  743 

saccular,  731 

strain  and,  732 

sympathetic  nerves  in,  741 

symptoms  of,  736 

syphilis  and,  732 

thrill  in,  746 

trachea  and,  742 

tracheal  tugging  in,  747 

tuberculosis  and,  739,  752 

tumors  and,  511 
761 


762 


INDEX 


Aneurism  of  aorta,  veins  and,  743 
vena  cava  andj  743 
X-rays  in,  749 
of  ascending  arch,  750 
of  descending  arch,  751 

thoracic  aorta,  752 
of  heart,  633 

of  innominate  artery,  756 
of  left  ventricle,  29 
of  sinuses  of  Valsalva,  750 
of  transverse  arch,  751 
physical  signs,  738 
rupture  into  auricles,  756 
into  pulmonary  artery,  756 
into  vena  cava,  756 
special  forms,  752 
symptoms,  738 
Aneurismal  varix,  731,  756 
Angina  pectoris,  708 
false,  713 
incipient,  712 
diagnosis,  713 
etiology,  712 
morbid  anatomy,  713   . 
physical  signs,  713 
symptoms,  713 
major,  708 

arterial  hypertension  in,  712 
diagnosis,  712 
etiology,  708 

intermittent  claudication  and,  709 
morbid  anatomy,  709 
physical  signs,  712 
symptoms,  710 
vasomotoria,  713 
diagnosis,  715 
etiology,  713 
morbid  anatomy,  714 
physical  signs,  715 
symptoms,  714 
pseudo-,  713 
sine  dolore,  711 
Angio-neurotic  edema,  479 
Angle,  Louis',  73 

subcostal,  27 
Anthracosis,  435 
Aorta,  aneurism  of,  731 

intrathoracic  tumors  and,  511 
arterio-sclerosis  of,  721 
atheroma  of,  721 
dilatation  of,  731,  752 
dynamic,  753 


Aorta,  dilatation  of,  etiology,  753 

morbid  anatomy,  753 

passive,  753 

physical  signs,  753 

symptoms,  753 
diseases  of,  716 
pulsation  of,  195 
rupture  of,  757 

morbid  anatomy,  757 

symptoms,  759 
Aortic  insufficiency,  676 

arterio-venous  signs  in,  681 

diagnosis,  681 

etiology,  676 

Graham  Steell  murmur  and,  681 

morbid  anatomy,  676 

murmur  of,  226 

pathological  physiology,  677 

physical  signs,  678 

symptoms,  678 

systolic  murmur  in,  680 
obstruction,  226 
roughening,  murmur  of,  226 
stenosis,  681 

diagnosis,  685 

etiology,  681 

morbid  anatomy,  682 

pathologic  physiology,  683 

physical  signs,  681 

symptoms,  684 

systolic  murmur  in,  684 

thrill  in,  684 
Aortitis,  acute,  716 

diagnosis,  718 

etiology,  716 

morbid  anatomy,  716 

physical  signs,  717 

Potain's  sign  in,  717 

symptoms,  717 
chronic,  721 

blood  pressure  m,  729 

etiology,  721 

morbid  anatomy,  723 

murmur  in,  730 

ophthalmoscope  in,  728 

physical  signs,  727 

retinal  vessels  in,  728 

sphygmomanometer  in,  728 

symptoms,  726 

syphilis  and,  723 
syphilitic,  718 

diagnosis,  721 


INDEX 


763 


Aortitis,  syphilitic,  etiology,  71S 
morbid  anatomy,  719 
physical  signs,  721 
symptoms,  719 
Apex  beat,  196 

displacement  of,  197 
pneumonia,  410 
Apoplexy,  pulmonary,  470 
Arch  of  aorta,  aneurism  of,  750 
Arrested  tuberculosis,  diagnosis,  352 
Arrhythmia,  cardiac,  168,  184 
in  children,  139 
heartblock,  169 
sinus,  169,  184 
Arterial  hypertension  in  angina  pectoris, 

712 
Arteries,  thickening  of,  155 
Arterio-sclerosis,  721 

chronic  endocarditis  and,  654,  655 
estimation  of,  155 
hypertrophy  of  heart  in,  623 
ophthalmoscope  in,  728 
retinal  arteries  in,  728 
sphygmomanometer  in,  728 
Arterio- venous  aneurism,  731,  756 
signs  in  aortic  insufficiency,  681 
Artery,  innominate,  aneurism  of,  756 

pulmonary,  atresia  of,  699 
Arthritis  in  tuberculosis,  327 
Aspergillosis,  pulmonary,  389 
diagnosis,  389 
etiology,  389 
morbid  anatomy,  389 
physical  signs,  389 
Aspiration  pneumonia,  393,  418 
Asthenic    conditions,    hemorrhagic    effu- 
sions and,  558 
pneumonia,  409 
Asthma,  breath  sounds  in,  119 
bronchial,  270 

anaphylaxis  and,  272 
chronic  heart  disease  and,  276 
diagnosis,  276 
etiology,  270 
exciting  causes,  271 
hay  fever  and,  271 
hypotheses  as  to  cause,  271 
nephritis  and,  276 
physical  signs,  275 
symptoms,  274 
urticaria  and,  275 
definition,  40 


Asthma,  fibrinous  bronchitis  and,  265 

Kopp's,  514 
Atelectasis,  445 

congenital,    broncho-pneumonia    and, 
426 

diagnosis,  448 

etiology,  445 

lobar  pneumonia  and,  414 

massive,  446 

morbid  anatomy,  446 

physical  signs,  448 

pleural  effusion  and,  449 
Atheroma  of  aorta,  721 
Athletics,  hypertrophy  of  heart  from,  621 
Atresia  of  pulmonary  artery,  699 
Atrophy  of  lungs,  454 
Auricles,  rupture  of,  aneurism  with,  756 
Auricular  fibrillation,  666,  673 
Auscultation,  extraneous  sounds,  105 

in  children,  139 

of  heart,  210,  222 

of  lungs,  104 
Azygos  vein,  hydrothorax  and,  565 

Baccelli's  sign,  551 

Bacteriology  of  broncho-pneumonia,  420 

of  lobar  pneumonia,  394 
Basilar  meningitis,  376 
Beer  heart,  623 
Bell  tympany,  69 
Biot's  breathing,  41 
Blastomycosis,  pulmonary,  3S4 
diagnosis,  387 
etiology,  384 
morbid  anatomy,  384 
physical  signs,  386 
skin  lesions  in,  385 
symptoms,  385 
Blood  in  lobar  pneumonia,  403 
Blood-pressure,  abnormal,  162 
estimation  of,  161 
in  aneurism,  749 
in  auricular  fibrillation,  174 
in  chronic  aortitis,  729 
in  lobar  pneumonia,  406 
in  tuberculosis  of  lungs,  325 
normal,  162,  729 
venous,  164 

Gaertner's  test,  77 
Blood-streaked  sputum    in    tuberculosis, 

313 
Botalli,  patent  ductus,  703 


764 


INDEX 


Bradycardia,  156,  628 
Brassy  cough  in  aneurism,  741 
Breath  sounds,  109 

absent,  114 

adventitious,  122 

amphoric,  119 

asthmatic,  119 

cavernous,  117 

cog-wheel,  121 

decreased,  114 

in  pleural  effusion,  115 

laryngeal  element,  109 

metamorphic,  119 

normal  and  abnormal,  113 

vesicular  element,  111 
Breathing,  bronchial,  origin  of,  61 
cavernous,  6,1 
cog-wheel,  340 
feeble,  340 
granular,  340 
stertorous,  40 
stridulous,  40 
type  of,  26 
Broadbent's  sign,  614,  745 
Bromin  gas,  481,  482 
Bronchi,  bilateral  differences  of,  48 
dilatation  of,  276,  310 
diseases  of,  257 
foreign  bodies  in,  287 
syphilis  of,  491 

diagnosis,  492 

morbid  anatomy,  491 

physical  signs,  492 

symptoms,  491 
Bronchial  asthma.     See  Asthma. 

breathing,  115 
Bronchiectasis,  276 

abscess  of  lung  and,  285,^464 
chronic  bronchitis  and,  285 
clubbing  of  fingers  and,  282 
compression  of  lung  and,  278 
diagnosis.  284 
dust  as  cause  of,  277 
dyspnea  in,  283 
etiology,  277 

fibrosis  of  lung  and,  278,  434 
foreign  body  and,  277 
gangrene  of  lung  and,  285 
loculated,  empyema  and,  285 
morbid  anatomy,  279 
physical  signs,  283 
pleuritis  and,  278 


Bronchiectasis,  pneumonia  and,  278 
Skoda's  veiled  puff  in,  284 
sputum  in,  282 
symptoms,  282 
syphilis  and,  278 
tuberculosis  and,  278,  284,  310 
Bronchiolectasis,  286 
diagnosis,  287 
etiology,  286 
morbid  anatomy,  286 
physical  signs,  286 
symptoms,  286  . 
tuberculosis,  acute,  and,  287 
Bronchiolitis  fibrosa  obliterans,  265 

diagnosis,  266 

etiology,  266 

morbid  anatomy,  266 

poisonous  gases  and,  266 

symptoms,  266 
Bronchitis,  acute,  257 

diagnosis,  259 

etiology,  257 

measles  and,  259 

morbid  anatomy,  258 

physical  signs,  258 

pneumonia  and,  259 

symptoms,  258 

tuberculosis  and,  315 

typhoid  fever  and,  259 

whooping  cough  and,  259 
chronic,  259 

bronchiectasis  and,  285 

diagnosis,  261 

etiology,  259 

morbid  anatomy,  260 

physical  signs,  261 

symptoms,  260 
fetid,  285 
fibrinous,  261 

asthma  and,  265 

diagnosis,  265 

etiology,  262 

foreign  body  and,  265 

morbid  anatomy,  262 

physical  signs,  264 

simple  bronchitis  and,  265 

symptoms,  264 
intrathoracic  tumors  and,  509 
putrid,  285 
Bronchophony,  132 
Broncho-pneumonia,  417 
atelectasis  and,  426 


IXDEX 


765 


Broncho-pneumonia,  bacteriology,  420 
bronchiectasis  and,  278 
bubonic  plague  and,  423 
complications.  426 
cough  in,  421 
diagnosis.  426 
duration,  423 
etiology,  417 
fever  in.  421 

gastro-intestinal  symptoms,  423 
lobar  pneumonia  and,  412 
morbid  anatomy,  419 
nervous  symptoms,  423 
pain  in,  421 
physical  sign,  424 
primary  form,  421 
protracted  form,  425 
pulse  in,  421 
secondary  form,  421 
sequels,  426 
skin  in.  422 
stage  of  complete  consolidation,  424 

of  congestion,  424 

of  partial  consolidation.  424 
symptoms.  420 
tuberculous,  426 
urine  in,  423 
Broncho-pneumonic  phthisis,  361 

morbid  anatomj-,  362 

physical  signs,  365 

symptoms,  364 
Bruit  de  Roger,  703 

de  tabourta,  718 
Bubonic  plague,  broncho-pneumonia   in. 
423 

California  disease,  387 

Cancer  of  lungs.  498 

Carbon  monoxide,  480 

Carcinoma  of  lung,  498 

Cardarelli's  sign,  747 

Cardiac  dilatation,   pericardial  effusion 
and.  610 
phenomena  in  tuberculosis,  342 
type  of  malignant  endocarditis,  649 

Cardiogram,  normal,  193 

Cardiorespiratory    murmurs,    247,     342. 
667 

Cardiovascular    symptoms    in    tubercu- 
losis, 325 

Carotid  murmurs,  246 

Cavernous  breathing.  117 


Cavity,  tuberculous,  pneumothorax  and, 
577 
signs  of,  348 
Central  pneumonia,  1 10 
Chalicosis,  436 

Change  of  note,  Biermer's,  72 

Friedreich's,  72 

Gerhardt's,  72 

Wintrich's,  72 

Charts,  graphic,  of  physical  signs.  146 

Chest,  barrel-shaped,  36 

bulging,  from  thoracic  aneurism,  30 

contour  and  mobility  of,  24 

deformity  in  heart  disease,  150 
in  tuberculosis,  310 

during  expiration,  24 

during  inspiration,  24 

emphysematous.  36 

expansion  of.  42 

in  rachitis,  32 

long,  flat,  36 

normal,  conformation  of,  22 

palpation  of,  42 

paralytic,  36 

pulsation,  27 

shape  of,  32 

size,  23 

topography,  22 

wall,  relation  of  pulmonary  lobes  to.  76 
valvular  areas  upon,  211 

wounds  of,  hemothorax  and.   559 
Cheyne-Stokes  respiration.  41 
Children,  lymph  nodes  in,  359 

physical  signs  in,  136 

pneumonia  in,  410 

pretuberculous,  360 

tuberculosis,  chronic,  in,  357 
Chills  in  tuberculosis,  324 
Chlorin  gas,  481,  482 
Chorea,  chronic  endocarditis  and.  654 

endocarditis  and,  641 
Chyliform  fluid,  563 
Chylothorax,  562 
Chylous  fluid.  562 

pseudo-,  563 
Circulatory  system,  examination-,  149 
Cirrhosis  of  lung.  427 
Clavicles,  prominence  of,  28 
Clinical  varieties  of  lobar  pneumonia,  409 
( Stubbing  of  fingers.  519 
bronchiectasis  and,  282 
in  congenital  heart  disease.  699 


766 


INDEX 


Clubbing  of  fingers  in  tuberculosis,  332 
pulmonary    osteo-arthropathy    and, 
526 
of  toes,  519 
Coccidioidal  granuloma,  387 
etiology,  387 
morbid  anatomy,  388 
physical  signs,  388 
symptoms,  388 
Cog-wheel  breathing,  121,  340 
Coin  test,  89 

in  pneumothorax,  574 
Colds,  tuberculosis  and,  315 
Collapse  of  lung,  414,  445 

massive,  446 
Compensation,  failing,  in  chronic  endo- 
carditis, 658 
in  heart  disease,  686 
in  chronic  endocarditis,  658 
Compensatory  emphysema,  456 
Congenital  heart  disease,  698 

pulmonary  stenosis,  699 
Congestion,  passive,  476 
etiology,  476 
morbid  anatomy,  476 
physical  signs,  477 
symptoms,  477 
pulmonary,  413,  475 
acute,  475 
etiology,  475 
morbid  anatomy,  475 
symptoms,  476 
poisonous  gases  and,  480 
Conjunctival  tuberculin  test,  355 
Consumption,  293.     See  also   Tuberculo- 
sis, pulmonary. 
Cor  bovinum,  677 

mobilis,  197 
Coronary  thrombosis,  myocarditis  due 

to,  627,  628 
Corrigan  pulse,  679 
Cough  in  broncho-pneumonia,  421 
in  intrathoracic  tumors,  505 
in  lobar  pneumonia,  402 
in  tuberculosis,  327 
Cracked  pot  sound,  69 
Crampton's  test,  177 
Creeping  pneumonia,  410 
Crepitant  rale  in  lobar  pneumonia,  406 
Crepitus  redux  in  lobar  pneumonia,  407 
Crisis  in  lobar  pneumonia,  404 
Croupous  pneumonia.     See  Pneumonia. 


Cutaneous  test  for  streptothricosis,  381 

tuberculin  test,  355 
Cyrtometer,  335 

Death  rattle,  40 
Decompensation  of  heart,  686 
Dermoid  cyst,  mediastinal,  507 
D'Espine's  sign,  361 
Dextrocardia,  706 
acquired,  35 
pseudo-,  706 
tuberculosis  and,  706 
Diaphragm,  579 
anatomy,  579 
diseases,  579 
empyema  and,  549,  592 
eventration  of,  588 

diagnosis,  590 

etiology,  589 

physical  signs,  590 

symptoms,  590 
evisceration  of,  etiology,  585 

physical  signs,  586 

symptoms,  586 
functional  disturbances  of,  582 
hernia  of,  585 

traumatic,  585 
hiccough  and,  560,  583 
hypertrophy,  581 
immobility,  592 
inflammation,  591 
inhibition,  582 
mobility,  28 
nerve  supply,  581 
paralysis,  583 
physiology,  102,  580 
pleural  effusions  and,  592 
position   of,   methods  of    determining, 

101 
scurvy  and,  591 
sneezing  and,  583 
spasm  of,  583 
tonic  spasm  of,  583 
trichiniasis  and,  591 
tuberculosis  and,  592,  596 
Diaphragmatic  hernia,  585 
pleurisy,  535 
shadow,  28 

sign  in  tuberculosis,  596 
Diaphragmatis,  591 
primary,  591 
secondary,  etiology,  591 


INDEX 


767 


Diaphragmatis,  secondary,  morbid  anat- 
omy, 592 
physical  signs,  595 
symptoms,  593 
Diarrhea  in  tuberculosis,  325 
Diastolic  murmur  in  mitral  stenosis,  674 
in  pulmonary  insufficiency,  695 
shock  in  aneurism,  746 
Diazo  reaction  in  tuberculosis,  326 
Digestive  symptoms  in  lobar  pneumonia, 

404 
Dilatation  of  aorta,  731 
of  heart,  624 

pericardial  effusion  and,  610 
Diphtheria,  myocarditis  and,  626 
Diseases  of  aorta,  716 
of  bronchi,  257 
of  diaphragm,  579 
of  lungs,  293 
of  myocardium,  617 
of  pericardium,  603 
of  pleura,  527 
Dissecting  aneurism,  731 
Distention  of  heart,  624 
Distomatosis,  pulmonary,  487 
diagnosis,  489 
etiology,  487 
morbid  anatomy,  488 
physical  signs,  489 
symptoms,  489 
tuberculosis  and,  489 
Double  pneumonia,  410 
Ductus  arteriosus,  patent,  703 

Botalli,  patent,  703 
Dulness,  66 

Duroziez,  murmur  of,  243,  680 
Dust,  crushed  slag,  437,  441 

inorganic,  and  pneumoconiosis,  435 

bronchiectasis  and,  277 
organic,  437 
Dysphagia  in  tuberculosis,  330 
Dyspnea,  39 

in  intrathoracic  tumors,  505 
in  tuberculosis,  330 
non-expansive,  40 

Echinococcus    cyst.     See    Hydatid   dis- 
ease. 

Edema,  angio-neurotic,  479 
in  chronic  endocarditis,  660 
of  lungs,  poisonous  gases  and,  480 
pulmonary,  478 


Edema,  pulmonary,  acute,  479 
morbid  anatomy,  479 
physical  signs,  479 
symptoms,  479 
chronic,  478 
etiology,  478 
morbid  anatomy,  478 
physical  signs,  479 
symptoms,  479 
Effusion,    pericardial,    intrathoracic    tu- 
mors and,  510 
Egophony,  135 

Electrocardiogram,  normal,  180 
Electrocardiograph,  principle  of,  179 
Emboli,  air,  471 
fat,  471 
infected,  471 

aneurism  and,  733 
Embolic  phenomena  in  endocarditis,  648 
Embolism,  pulmonary,  470 
Emphysema,  449 

chronic  hypertrophic,  449 
etiology,  449 
heredity,  450 
morbid  anatomy,  451 
occupation  and,  450 
physical  signs,  453 
symptoms,  452 
compensatory,  456 

physical  signs,  456 
interstitial,  455 
senile,  454 
,  small  lunged,  454 

morbid  anatomy,  455 
physical  signs,  455 
symptoms,  455 
subcutaneous,  518 
vesicular,  acute,  455 
vicarious,  456 
Empyema,  544 

Baccelli's  sign  in,  551 
diagnosis,  551 
diaphragm  and,  549,  592 
encapsulated,  551 
encysted,  551 
etiology,  545 
loculated,  551 

bronchiectasis  and,  285 
diagnosis,  556 
etiology,  552 
morbid  anatomy,  554 
physical  signs,  556 


768 


INDEX 


Empyema,  loculated,  pneumonia  and,  556 

symptoms,  555 

tuberculosis  and,  556 
morbid  anatomy,  545 
necessitatis,  518,  548,  550 
physical  signs,  127,  549 
pulsating,  550 
symptoms,  549 
Endocarditis,  640 
acute,  640 

chorea  and,  641 

chronic  diseases  and,  641 

etiology,  640 

morbid  anatomy,  641 

physical  signs,  642 

rheumatic  fever  and,  640 

symptoms,  642 

tonsillitis  and,  641 
chronic,  654 

arterio-sclerosis  and,  654,  655 

chorea  and,  654 

compensation  in,  658 

congenital,  655 

decompensation  in,  658 

edema  in,  660 

etiology,  654 

gastro-intestinal  symptoms,  661 

goitre  and,  655 

infectious,  651 
anemia  in,  653 
diagnosis,  654 
morbid  anatomy,  651 
physical  signs,  653 
symptoms,  651 

jaundice  in,  661 

morbid  anatomy,  655 

murmurs  in,  658 

nephritis  and,  655 

pathological  physiology,  656 

rheumatic  fever  and,  654,  655 

symptoms,  659 

syphilis  and,  655 

tonsillitis  and,  654 

ulcerative,  651 
gonorrheal,  694 
lobar  pneumonia  and,  399 
malignant,  644 

cardiac  type,  649 

chronic,  651 

diagnosis,  650 

embolism  in,  645, '648 

etiology,  644 


Endocarditis,  malignant,  miliary  tuber- 
culosis and,  375 
morbid  anatomy,  644 
physical  signs,  649 
pyemic  form,  649 
symptoms,  647 
tuberculosis  and,  650 
typhoid  form,  649,  650 
neural,'  647 

subacute  bacterial,  651 
ulcerosa,  644 
Eosinophilia  in  hemorrhagic  effusions,  557 
Epidemics  of  pneumonia,  392,  410 
Esophagus,  aneurism  of  aorta  and,  741 
Eustace  Smith's  sound,  247 
Eventration  of  diaphragm,  588 
Evisceration  of  diaphragm,  585 
Ewart's  sign  of  pericardial  effusion,  251 
Exaggerated  breathing,  113 
Examining  cape,  21 
Exercise,    physical,    murmurs    resulting 

from,  241 
Exophthalmic     goitre,     hypertrophy     of 

heart  in,  623 
Expansion  of  chest,  unequal,  24 

of  lungs,  direction,  25 
Expectoration  in  tuberculosis,  327 
Extrasystoles,  171,  184 

Fat  emboli,  471 

Fatty  degeneration  of  heart,  630 

infiltration  of  heart,  631 
Fetid  bronchitis,  285 
Fetus,    infection    of,    with    tuberculosis, 

294 
Fever  in  broncho-pneumonia,  421 
in  lobar  pneumonia,  400 
in  tuberculosis,  317 
Fibrillation,  auricular,  173,  186 
Fibrinous  bronchitis,  261 
Fibroid  phthisis,  367 
Fibrosis  of  lung,  bronchiectasis  and,  278 
syphilis  and,  493 
pulmonary,  427 

bronchiectasis  and,  434 
diagnosis,  432 
etiology,  427 
morbid  anatomy,  428 
physical  signs,  432 
Finger  nails,  curved,  519 

oyster  shell,  519 
Fingers,  clubbing  of,  519 


INDEX 


769 


Fingers,  clubbing  of,  in  congenital  heart 

disease,  699 
Fistula  in  ano  in  tuberculosis,  315 
Flatness,  68 

Flint's  murmur,  244,  675,  680 
Flutter,  auricular,  173,  188 
Foramen  ovale,  patent,  699 
Foreign  bodies,  bronchiectasis  and,  277 
fibrinous  bronchitis  and,  265 
in  air  passages,  287 
diagnosis,  291 
etiology,  287 
morbid  anatomy,  288. 
physical  signs,  291 
symptoms,  290 
tuberculosis  and,  291 
Fremitus,  tactile,  45 

vocal,  45 
Friction,  pleural,  52 
sound,  pericardial,  249 
pleural,  125 
Frictions,  122 

Friedlander's  bacillus  pneumonia,  414 
diagnosis  of,  415 
etiology,  414 
morbid  anatomy,  414 
physical  signs,  415 
symptoms,  414 
Funnel  breast,  35 

Gallop  rhythm,  presystolic,  218 
["•■-      protodiastolic,  219 
Galloping  consumption,  361 
Gangrene,  pulmonary,  466 

bronchiectasis  and,  285 

circumscribed,  467 

diagnosis,  469 

diffuse,  468 

etiology,  466 

morbid  anatomy,  467 

physical  signs,  469 

symptoms,  469 
Garland's  triangle,  538 
Gas  bacillus  infection  of  hemothorax,  561, 

562 
Gases,  poisonous,  480 
Gassing,  480 

Gastro-intestinal  symptoms  in  broncho- 
pneumonia, 423 

in  tuberculosis,  316,  324 

in  endocarditis,  661 
tract  in  tuberculosis,  311 

49 


Goitre  and  enlarged  thymus,  513,  517 

chronic  endocarditis  and,  655 

exophthalmic,    hypertrophy    of  heart 
in,  623 

murmurs  in,  246 
Gold  miner's  phthisis,  441 
Gonorrheal  endocarditis,  694 
Graham  Steell  murmur,  681,  695 
Granular    breathing    in    tuberculosis    of 

lungs,  340 
Grocco's  triangle,  540 
Groove,  Harrison's,  34 
Gummata  in  syphilis  of  lungs,  493 
Gunn's  vessels,  728 
Gunshot  wounds  of  chest,  559 

Hay  fever,  bronchial  asthma  and,  271 
Head's  areas,  43 

Heart,  anatomical  considerations    151 
aneurism  of,  633 
etiology,  633 
morbid  anatomy,  633 
physical  signs,  634 
symptoms,  634 
auscultation  of.  210 
brown  atrophy  of,  631 
characteristic    percussion    outlines    in 

disease,  205 
chronic  valvular  disease  of,  654 
crunching  sound  of,  215 
decompensation,  picture  of,  244 
dilatation  of,  624 

pericardial  effusion  and,  610 
physical  signs,  625 
symptoms,  625 
disease,  bronchial  asthma  and,  276 
congenital,  698 

clubbing  of  fingers  in,  699 
hydrothorax  and,  564 
polycythemia  in,  698 
pulmonary  infarction  and,  470 
symptoms,  625 
tuberculosis  and,  343 
hydrothorax  and,  564 
distention  of,  624 
dulness,  deep,  203 

method  of  recording,  206,  207 
normal,  202 
significance  of,  204 
superficial,  203 
examination,  practical   considerations, 
253 


770 


INDEX 


Heart,  failing  compensation  of,  6S6 
fatty,  630 

degeneration  of,  630 
infiltration  of,  631 
hypertrophy  of,  617 

adhesive  pericarditis  and,  623 
and  dilatation  (frozen  section),  243 
arterio-sclerosis  and,  623 
athletics  and,  621 
left  ventricular,  216 
Munich  beer  heart  and,  623 
nephritis  and,  623 
pathological,  622 
physical  signs,  623 
symptoms,  623 
physiological,  621 
physical  signs,  621 
symptoms,  621 
pregnancy  and,  621 
tachycardia  and,  623 
valvular  disease  and,  622 
impulse,  193 

displacement  of,  197 
in  infancy,  138 
in  tuberculosis,  310,  345,  346 
Munich  beer,  623 
murmurs,  220 

functional,  240 
muscular  tonicity  of,  625 
normal  impulse,  196 
outlines,  208 
position,  151 
rhythm,  168 
percussion,  200 
position,  194 

in  pericardial  effusion,  252 
posterior  view,  99,  100 
soldier's,  177,  191 
acoustics  of,  212 
changes  in  pitch,  217 
disproportion  of,  215 
in  children,  141 
individual  variation  of,  214 
intensity,  222 
origin  and  character  of,  210 
production,  213 
reduplication  of,  217 
rhythm  of,  218 
syphilis  of,  636 
diagnosis,  639 
morbid  anatomy,  636 
symptoms,  637 


Heart  valves,  anatomic  relations,  152 

valvular  lesions,  combined,  656 
Heart-block,  169,  187 
Hematoma  of  pleura,  559 
Hemopericardium,  607 
Hemoptjrsis,  causes,  314 
in  aneurism  of  aorta,  743 
in  pulmonary  tuberculosis,  313,  328 
Hemothorax,  559 
diagnosis,  562 
etiology,  559 

gas  bacillus  infection  of,  561,  562 
infection,  561 
non-traumatic,  559 
physical  signs,  561 
symptoms,  560 
traumatic,  559 
Hemorrhagic  pleural  effusions,  557 
Heredity,  tuberculosis  and,  295 
Hernia,  diaphragmatic,  585 
of  lungs,  517 

subcutaneous  emphysema  and,  518 
Herpes  zoster  in  tuberculosis,  326 
Hiccough,  560,  583 

Hoarseness,  tuberculosis  and,  315,  329 
Hodgkin's    disease,  intrathoracic  tumor 

and,  512 
Hydatid  disease,  484 
diagnosis,  486 
etiology,  484 

malignant  tumor  and,  487 
morbid  anatomy,  484 
of  lungs,  484 
of  pleura,  484 
physical  signs,  486 
pleural  effusion  and,  487 
symptoms,  485 
tuberculosis  and,  487 
Hydrochloric  acid  fumes,  481 
Hydropericardium,  607 
Hydropneumothorax,      physical      signs, 

126 
Hydrothorax,  133,  564 
azygos  vein  and,  565 
compression  of  lung  in,  120 
etiology,  564 
frozen  section  of,  239 
heart  disease  and,  564 
morbid  anatomy,  564 
physical  signs,  567 
pulmonary  veins  and,  566 
symptoms,  566 


INDEX 


771 


Hyperesthesia,  cutaneous,  43 

in  tuberculosis,  326 
Hypernephroma  of  lungs,  499 
Hyperresonance,  66 
Hypertension,  164 
Hypertrophic    pulmonary    osteo-arthro- 

pathy,  522 
Hypertrophy,    left    ventricular,    prepon- 
derating, 182 

of  heart,  617 

of  lungs,  456 
Hypostatic  congestion,  476 
Hypotension,     Jacquet     cardiosphygmo- 

graph,  163 

Imperforate  ventricular  septum,  702 
Indian,  tuberculosis  and,  295 
Infant,  chest  of,  142,  143 

physical  findings  in,  136 
Infarction,  pulmonary,  413,  470 

air  emboli  and,  471 

diagnosis,  474 

etiology,  470 

fat  emboli  and,  471 

foreign  material  and,  471 

heart  disease  and,  470 

infected  emboli  and,  471 

malignant  disease  and,  474 

morbid  anatomy,  471 

phlebitis  and,  470 

physical  signs,  474 

pneumonia  and,  474 

symptoms,  473 

tuberculosis  and,  474  • 

Infections,  tuberculosis  and,  297 
Infective  endocarditis,  acute,  644 
Influenza,  myocarditis  and,  627 
Ingestion,  tuberculosis  by,  294 
Inhibition  of  diaphragm,  582 
Inhalation  pneumonia,  393 

tuberculosis  from,  294 
Innominate  artery,  aneurism  of,  756 
Insanitary    conditions    and    pneumonia, 
392 

surroundings  and  tuberculosis,  296 
Inspection,  general,  19 

in  circulatory  disease,  149 

of  chest,  17,  20 
Intercostal  neuralgia,  pleurisy  and,  543 
Intermittent  claudication,  709 
Interstitial  pneumonia,  427 


Interventricular  septum,  patulous,  246 
Intrathoracic  tumors,  498 

aneurism  and,  511 

bronchitis  and,  509 

constitutional  symptoms  in,  506 

cough  in,  505 

diagnosis,  509 

dyspnea  in,  505 

etiology,  498 

expectoration  in,  505 

Hodgkin's  disease  and,  512 

inflammation  of  lungs  and,  509 

leukemia  and,  512 

morbid  anatomy,  499 

onset  in,  505 

pain  in,  505 

pericardial  effusion  and,  510 

physical  signs,  508 

pleural  effusion  and,  509 

pressure  symptoms,  506 

primary,  498,  500 

secondary,  499,  503,  508 

symptoms,  504 

tuberculosis  and,  509 
Iodide  of  potassium  in  tuberculosis,  355 
Irrespirable  gases,  480 
Ischio-rectal  abscess  in  tuberculosis,  315 
fossa  in  tuberculosis,  311 

Jaundice  in  chronic  endocarditis,  661 

in  tuberculosis,  325 
Jugular  veins,  pulsation  in,  687 

Kidneys  in  tuberculosis,  312 
Kopp's  asthma,  514 
Kronig's  isthmus,  337 
Kyphoscoliosis,  30,  39 

Larval  pneumonia,  409 
Laryngeal  nerve  in  aneurism  of  aorta,  741 
paralysis  of  recurrent,  671,  676 

sounds,  109 
Larynx  in  tuberculosis,  311 

syphilis  of,  490 
Leukemia,  intrathoracic  tumors  and,  512 
Litten's  phenomenon,  28 
Liver,  examination  of,  by  palpation,  51 

pericardial  pseudo-cirrhosis  of,  615 
Lobar  pneumonia,  391 
Louis'  law  in  tuberculosis,  317 
Lungs,  abscess  of,  458 

and  bronchiectasis,  285 


772 


INDEX 


Lungs,  amount  of  air  in,  92 

anatomic  considerations,  73 

aneurism  of  aorta  and,  742 

apices,  expansion  of,  101 
percussion  of,  97 

atelectasis  of,  124 

atrophy  of,  454 

auscultation  of,  104 

border  in  pneumothorax,  576 

brown  induration  of,  671 

carcinoma  of,  498 

cirrhosis  of,  427 

collapse  of,  414 

compression  of,  and  bronchiectasis,  278 
in  children,  144 

diseases  of,  293 

examination  of,  19 

gangrene  of,  466 

bronchiectasis  and,  285 

hernia  of,  517 

hydatid  disease  of,  484 

hypernephroma  of,  metastases  in,  499 

hypertrophy  of,  456 

infarction  of,  470 

inferior  margin  of,  99 

lobes  of,  in  relation  to  chest  wall,  76 

malignant  deciduoma  in,  499 
disease  of,  474,  498,  543 

mycotic  infections  of,  378 

normal  shape  of,  74 

poisonous  gases  and,  480 

practical    considerations    in    examina- 
tion, 144 

reflexes,  72 

sarcoma  of,  498 

superior  margin  of,  97 

syphilis  of,  492 

traction  of,  103 

tuberculosis  of,  293 
Lymph  nodes  in  children,  359 

tracheo-bronchial,  tuberculosis  of,  360 

Malaise  in  tuberculosis,  323 
Malaria,  tuberculosis  of  lungs  and,  317 
Malignant  deciduoma  of  lungs,  499 
disease  of  lungs,  474,  498,  543 
hemorrhagic  effusions  and,  558 
of  mediastinum,  498 
of  pleura,  498,  503,  543 
endocarditis,  644 
tumor,  hydatid  disease  and,  487 
Marital  infection  in  tuberculosis,  294 


Massive  pneumonia,  410 

Measles,  acute  bronchitis  and,  259 

whooping  cough  and,  270 
Mediastinal   tumor,    aneurism    of   aorta 

and,  752 
Mediastino-pericarditis,  613 
Mediastinum,  benign  tumors  of,  503 
dermoid  cyst  of,  507 
malignant  disease  of,  498 
middle  view  of,  197 
tumors  of,  499 
Meningeal  form  of  miliary  tuberculosis, 

376 
Meninges  in  tuberculosis,  312 
Meningitis,  basilar,  376 
lobar  pneumonia  and,  399,  414 
tuberculous,  376 
etiology,  376 
morbid  anatomy,  376 
symptoms,  377 
Menstrual  function  in  tuberculosis,  316, 
327 
period  in  tuberculosis,  319 
Mental  attitude  in  tuberculosis,  326 
Mesaortitis,  718 
Metallic  ring,  69 
tinkle,  129 

in  pneumothorax,  574 
Miliary  tuberculosis.     See    Tuberculosis, 

miliary. 
Miners'  phthisis,  435 
Mitral  insufficiency,  661 

auricular  fibrillation  in,  666 

broken  compensation  in,  665 

cardio-respiratory  murmur  in,  667 

diagnosis  of,  667 

etiology,  661 

morbid  anatomy,  662 

murmur,  228 

pathologic  physiology,  664 

physical  signs,  665 

pulmonary  systolic  murmur  in,  667 

relative,  661 

murmur  in,  667 
sj^mptoms,  664 
obstruction,  chest  deformity  due  to, 
150 
murmur  of,  229 
regurgitation,  661 
stenosis,  667 

aneurism  and,  676 
of  aorta  and,  752 


INDEX 


773 


Mitral  stenosis,   auricular  fibrillation  in, 
673 

ball  thrombus  in,  670 

brown  induration  of  lung  in,  671 

diagnosis,  675 

diastolic  murmur  in,  674 

etiology,  667 

first  sound  in,  674 

Flint's  murmur  in,  675 

morbid  anatomy,  667 

obstruction,  buttonhole,  236 
funnel-shaped,  237 

paralysis  of  laryngeal  nerve  in,  671, 
676 

pathologic  physiology,  669 

physical  signs,  672 

presystolic  murmur  in,  673 
thrill  in,  672 

pseudo-tuberculous  type,  872 

pulmonary  insufficiency  in,  674 

stages,  675 

symptoms,  671 

systolic  murmur  in,  674 

tuberculosis  and,  672,  676 
Moritz's  conjugates,  207 
Moro  tuberculin  test,  355 
Munich  beer  heart,  623 
Mural  endocarditis,  645 
Murmurs  after  physical  exertion,  241 
cardio-respiratory,  247,  342,  667 
diastolic,  in  mitral  stenosis,  674 

in  pulmonary  insufficiency,  695 
Duroziez's,  243,  680 
effect  of  respiration  upon,  242 
endocardial,  223 
exocardial,  246 
Flint's,  244,  675,  680 
functional,  240 

distribution  of,  248 

in  childhood,  144 
Graham  Steell,  681,  695 
hepatic,  248 

in  chronic  endocarditis,  658 
individual,  valvular,  226 
of  aortic  insufficiency,  226 

obstruction,  226 
of  mitral  insufficiency,  228 

obstruction,  229 
of  pulmonary  insufficiency,  235 

stenosis,  234 
of  relative  insufficienc}',  667 
of  tricuspid  insufficiency,  232 


Murmurs  of  tricuspid  stenosis,  234 
pleuro-pericardial  friction,  605 
presystolic,  673 
pulmonary  systolic,  667 
result  of  persistent  thymus,  247 
Roger's,  246,  703 
special  varieties  of,  243 
subclavian,  342 
systolic,  in  aortic  insufficiency,  680 

in  aortitis,  730 

in  mitral  stenosis,  674 
Traube's,  244 

valvular,  differentiation,  224 
vascular,  246 
venous,  247 
Muscles,  rigidity  of,  in  tuberculosis,  334 
Mycotic  aneurisms,  733 

infections  of  lungs,  378 
Myocardial  changes  due  to  syphilis,  636 
Myocarditis,  626 

coronary  thrombosis  and,  627,  628 

diagnosis,  629 

diphtheria  and,  626 

etiology,  626 

influenza  and,  627 

interstitial,  627 

morbid  anatomy,  627 

physical  signs,  628 

rheumatic  fever  and,  626 

suppurative,  627 

symptoms,  628 

syphilis  and,  627 

typhoid  fever  and,  627 
chronic,  629 

acidosis  in,  632 

diagnosis,  633 

etiology,  629 

fatty,  630 

fibrous,  630 

morbid  anatomy,  630 

physical  signs,  632 

symptoms,  631 
Myocardium,  abscess  of,  627 
diseases  of,  617 
interstitial  changes  in,  627 
parenchymatous  degeneration  of,  627 

Nails,  finger,  curved,  518 

oyster  shell,  519 
Negro,  tuberculosis  and,  295 
Nephritis,  endocarditis  and,  655 
hypertrophy  of  heart  in.  623 


774 


INDEX 


Nervous     symptoms    in    broncho-pneu- 
monia, 423 
in  lobar  pneumonia,  403 
system  in  tuberculosis,  326 
Neuralgia,  intercostal,  pleurisy  and,  543 
Neurasthenia,  tuberculosis  and,  323 
Night  sweats  in  tuberculosis,  324 
Nitric  acid  fumes,  480,  483 
Nitrous  acid  fumes,  480,  483 
Normal  percussion  findings,  94 

Occupation,  lobar  pneumonia  and,  394 
tuberculosis  and,  297 

Oliver's  sign,  747 

Ophthalmoscope  in  arterio-sclerosis,  728 

Orthodiagraph,  208 

Orthopercussion,  201 

Orthopnea,  39 

Osteo-arthropathy,  hypertrophic  pulmon- 
ary, 522 

Overtones,  53,  56 

Oyster  shell  finger  nails,  519 

Pain  in  broncho-pneumonia,  421 

in  tuberculosis  of  lungs,  329 

pleural,  44 

reflex,  43 
Palpation  of  abdomen,  51 

of  chest,  42 

of  precordium,  193 

of  pulse,  155 
Paralysis  of  diaphragm,  583 

of  laryngeal  nerve  by  aneurism,  741 

of  recurrent  laryngeal  nerve,  671,  676 
Pararythmia,  169 
Patent  ductus  arteriosus,  703 

foramen  ovale,  699 
Pathologic  hypertrophy  of  heart,  622 
Pectoriloquy,  132 

whispered,  in  children,  140 
Percussion,  auscultatory,  90 

depth  of  penetration,  83 

dulness,  due  to  full  stomach,  90 

history,  63 

in  infants,  136 

methods,  79 

of  heart,  200 

of  lungs,  normal  variations,  94 

outline  of  heart  in  disease,  205 

purpose,  86 

resistance,  87 

results,  79,  81 


Percussion  sounds,  effect  of  spinal  curva- 
ture on,  93 
conditions  modifying,  90 
special,  72 
special  varieties,  88 
technic,  88 
theory  of,  63  ' 
threshold,  89 
Percutaneous  tuberculin  test,  355 
Pericardial  effusion,  208,  607 
cardiac  dilatation  and,  610 
diagnosis,  610 

displacement  of  heart  by,  198 
frozen  section  of,  243 
intrathoracic  tumors  and,  510 
morbid  anatomy,  607 
physical  signs,  608 
pulsus  paradoxus  in,  609 
Rotch's  sign  in,  609 
symptoms,  608 
pseudo-cirrhosis  of  liver,  615 
Pericarditis,  acute  fibrinous,  603 
diagnosis,  605 
etiology,  603 
morbid  anatomy,  603 
physical  signs,  605 
symptoms,  604 
adhesive,  252,  610 
Broadbent's  sign,  614 
Flint's  murmur  in,  675 
hypertrophy  of  heart  in,  623 
morbid  anatomy,  611 
pathological  physiology,  613 
physical  signs,  614 
symptoms,  613 

systolic  retraction  of  interspaces  in, 
"  614 

varieties,  611 
friction  sound  in,  249 
lobar  pneumonia  and,  398 
mediastino-,  613 
serofibrinous,  illustration,  249 
tuberculous,  603,  606 
with  effusion,  251 
frozen  section  of,  250 
position  of  heart  in,  252 
Pericardium,  diseases  of,  603 
Peritonitis,  subphrenic,  596 
Pernicious  endocarditis,  644 
Pertussis.     See  Whooping  cough. 
Phlebitis,  pulmonary  gangrene  and,  470 
Phlebogram,  normal,  168 


INDEX 


775 


Phrenic  nerve  in  aneurism,  741 

wave,  28 
Phthisis.     See  also  Tuberculosis  of  lungs. 
Physical  signs  as  affected  by  posture,  106 

graphic  records  of,  145,  146 
Physiologic  hypertrophy  of  heart,  621 
Physiology  of  diaphragm,  580 
Pick's  disease,  615 
Pigeon  breast,  35 
Pitch  of  heart  sounds,  217 

of  sound,  58 
Pleura,  diseases  of,  527 
hematoma  of,  559 
hydatid  disease  of,  484 
inflammation  of,  and  bronchiectasis, 

278 
malignant  disease  of,  498,  503,  543 
thickening  of,  544 
Pleural  effusion,  529,  532 
atelectasis  and,  449 
breath  sounds  in,  115 
diagnosis,  543 
diaphragm  and,  592 
exploratory  puncture  in,  542 
Grocco's  triangle  in,  540 
hemorrhagic,  557 

asthenic  conditions  and,  558 
eosinophilia  in,  557 
idiopathic,  558 
malignant  disease  and,  558 
thoracentesis  and,  559 
tuberculosis  and,  557 
hydatid  disease  and,  487 
in  children,  141 
intrathoracic  tumors  and,  509 
lobar  pneumonia  and,  412 
malignant  disease  and,  543 
movable  dulness  in,  539 
physical  signs,  535 

after  absorption,  542 
pneumothorax  and,  578 
pressure  effects  of,  531 
pain,  44 

space,  obliteration  of,  in  tuberculosis, 
309 
Pleurisy,  527 
chronic,  544 
cough  in,  532 
diagnosis,  543 
diaphragmatic,  535 
dry,  533 

physical  signs,  533 


Pleurisy,  etiology  of,  527 

fibrinous,  528,  534 
physical  signs,  534 

intercostal  neuralgia  and,  543 

malignant  disease  and,  543 

morbid  anatomy,  528 

pain  in,  532 

physical  signs,  533 

pleurodynia  and,  543 

pneumonia  and,  543 

purulent,  544 

respirations  in,  532 

serofibrinous,  529 

serous,  529 

symptoms,  532 

tuberculosis  and,  315,  527 

with  effusion,  529,  532 
Pleuritic    friction    rub    in    tuberculosis, 

345 
Pleurodynia,  543 

pleurisy  and,  543 
Pleuro-pericardial  friction,  605 
Plexor  and  pleximeter,  80 
Pneumococcus,  types,  394 
Pneumoconiosis,  434 

diagnosis,  444 

dust,  inorganic,  and,  435 
organic,  and,  437 

etiology,  435 

macroscopic  changes  in,  440 

microscopic  changes  in,  439 

morbid  anatomy,  439 

physical  signs,  443 

symptoms,  442 

tuberculosis  and,  438 
Pneumonia,  abortive,  409 

acute  bronchitis  and,  259 

apex,  410 

aspiration,  418 

asthenic,  409 

bronchiectasis  and,  278 

broncho-,  417 

central,  410 

chronic,  427 

creeping,  410 

double,  410 

epidemic,  410 

Friedlander's  bacillus,  414 

in  alcoholic  subjects,  409 

in  children,  410 

interstitial,  427 

larval,  409 


776 


INDEX 


Pneumonia,  lobar,  391 
aspiration,  393 
associated  lesions  in,  398 
atelectasis  and,  414 
bacteriology,  394 
blood  in,  403 
blood-pressure  in,  406 
broncho-pneumonia  and,  412 
chronic  diseases  and,  393 
clinical  varieties,  409 
collapse  in,  409 
cough  in,  402 
crepitant  rales  in,  406 
crepitus  redux  in,  407 
crisis  in,  404 
diagnosis,  411 
digestive  symptoms,  404 
endocarditis  and,  399 
epidemics,  392 
etiology,  391 
fever  in,  400 

gray  hepatization  and,  396 
in  children,  410 
inhalation,  393 

insanitary  conditions  and,  392 
loculated  empyema  and,  556 
meningitis  and,  399,  414 
morbid  anatomy,  396 
nervous  symptoms  in,  403 
pericarditis  and,  398 
personal  conditions  and,  393 
physical  signs,  405 
pleurisy  and,  543 
pneumonic  phthisis  and,  367 
post-operative,  393 
previous  attacks,  393 
pulmonary  congestion  and,  413 

infarction  and,  413,  474 
red  hepatization  and,  396 
resolution  of,  397 
respiratory  symptoms,  402 
seasonal  incidence,  392 
site  of  disease,  398 
skin  in,  404 
sputum  in,  403 
stage  of  engorgement,  396 

of  resolution,  408 
symptoms,  399 
trauma  and,  393 
tuberculosis  and,  322 
tuberculous  pneumonia  and,  412 
typhoid  fever  and,  414 


Pneumonia,  lobar,  urine  in,  404 
X-ray  findings  in,  411 
massive,  410 
postoperative,  410 
secondary,  411 
senile,  409 
terminal,  409 
tuberculous,  366,  412 
typhoid,  409 
wandering,  410 
Pneumonic  phthisis,  366,  412 
diagnosis,  367 
lobar  pneumonia  and,  367 
morbid  anatomy,  366 
physical  signs,  367 
symptoms,  366 
Pneumonocele,  517 
Pneumothorax,  568 

characteristic  signs,  575 
coin  test  in,  574 
diagnosis,  576 
etiology,  568 
insidious  onset,  573 
lung  border  in,  576 
metallic  tinkle  in,  574 
morbid  anatomy,  568 
partial,  575 
physical  signs,  572 
pleural  effusion  and,  578 
spontaneous,  572 
succussion  splash  in,  574 
symptoms,  572 
tuberculosis  and,  568 
tuberculous  cavity  and,  577 
Poisonous     gases,     bronchiolitis     fibrosa 
obliterans  and,  266 
effects  of,  on  respiratory  tract,  480 
diagnosis,  484 
morbid  anatomy,  481 
physical  signs,  483 
symptoms,  482 
Polycythemia   in    congenital   heart   dis- 
ease, 698 
in  tricuspid  stenosis,  693 
Post-operative  pneumonia,  393,  410 
Posture,  influence  of,  on  physical  signs, 
106 
in  physical  examination,  21 
Potain's  sign  in  aortitis,  717 
Potter's  phthisis,  436 
Pregnancy,  heart  in,  621 
tuberculosis  and,  298 


INDEX 


777 


Presystolic  murmur,  673 

thrill,  672 
Pretuberculous  children,  360 
Pseudo-angina,  713 
Pseudo-chylous  fluid,  563 
Psittacosis,  416 
diagnosis,  417 
etiology,  416 
morbid  anatomy,  416 
physical  signs,  417 
symptoms,  417 
Puerperal  period,  tuberculosis  and,  298 
Pulmonary  actinomycosis,  381 
apoplexy,  470 
artery,  atresia  of,  699 

rupture  of  aneurism  into,  756 
aspergillosis,  389 
blastomycosis,  384 
congestion,  413,  475 
distomatosis,  487 
edema,  477 
embolism,  470 
fibrosis,  427 
gangrene,  466 
infarct,  413,  470 
insufficiency,  235,  693 

diagnosis,  695 

etiology,  693 

gonorrhea  and,  694 

mitral  stenosis  and,  674 

morbid  anatomy,  694 

pathologic  physiology,  694 

physical  signs,  695 

symptoms,  694 
osteo-arthropathy,  acromegaly  and,  526 

clubbing  of  fingers  and,  526 

diagnosis,  526 

etiology,  522 

morbid  anatomy,  523 

symptoms,  524 
sporotrichosis,  390 
stenosis,  695 

congenital,  699 

diagnosis,  696 

etiology,  695 

morbid  anatomy,  696 

murmur  of,  234 

pathologic  physiology,  696 

physical  signs,  696 

symptoms,  696 
streptothricosis,  378 
symptoms  of  trichuriasis,  591 


Pulmonary  systolic  murmurs,  667 

tension,  changes  in,  92 

tuberculosis.    See  Tuberculosis  of  lungs. 

veins,  hydrothorax  and,  566 
Pulsation,  epigastric,  196 

of  aneurism,  747 
Pulse,  alternation  of,- 175,  190 

arterial,  normal,  157 

bigeminal,  158 

character,  155 

dicrotic,  158 

equality,  157 

in  broncho-pneumonia,  421 

intermittent,  171 

irregularities,  168,  184 

palpation,  155 

paradoxic,  158 

rate,  156 

tension,  156 

tracings,  interpretation,  167 

venous,  normal,  164 

volume,  156 

water-hammer,  158 
Pulsus  alternans,  175,  190 

bisferiens,  158 

paradoxus,  609 
Purpura  in  tuberculosis,  325 
Putrid  bronchitis,  285 
Pyemic  form  of  endocarditis,  649 
Pyopneumothorax  subphrenicus,  597,  600 
Pyothorax,  544 

Rachitic  chest,  32 
Rales,  122 

latent,  125 

significance,  125 
Reduplication  of  heart  sounds,  217 
Regurgitation,  aortic,  676 

mitral,  661 

pulmonary,  693 

tricuspid,  685 
Relapse  in  lobar  pneumonia,  409 
Resistance,  sense  of,  87 
Resolution,  stage  of,  in  lobar  pneumonia, 

397,  408 
Resonance,  59 

percussion,  65 

vocal,  130 
Resonators,  56 
Respiration,  Biot's,  41 

Cheyne-Stokes,  41 

effect  of,  on  heart  murmurs,  242 


778 


INDEX 


Respiration,     pressure     changes    during, 
103 
rate,  27 

in  broncho-pneumonia,  421 
restricted,  40 
type,  26 
Respiratory  sounds,  109 

symptoms  in  lobar  pneumonia,  402 
tract,  poisonous  gases  and,  480 
syphilis  of,  490 
Retinal  arteries  in  arterio-sclerosis,  728 
Rheumatic    fever,    chronic    endocarditis 
and,  654,  655 
endocarditis  and,  640 
myocarditis  and,  626 
Roentgen  ray.     See  X-ray. 
Roger's  murmur,  246,  703 
Rotch's  sign  of  pericardial  effusion,  251, 

609 
Rupture  of  aneurism,  756 
of  aorta,  757 

Sarcoma  of  lung,  498 

Scoliosis,  effect  of,  in  percussion,  92 

Scurvy,  diaphragm  in,  591 

Secondary  pneumonia,  411 

Senile  pneumonia,  409 

Septic  endocarditis,  644 

Serositis,  multiple,  615 

Sex,  effect  of,  percussion  of  chest,  101 

Shock,  diastolic,  196 

Shoddy  fever,  438 

Siderosis,  436 

Silicosis,  436 

Sinus  arrhythmia,  169 

Sinuses  of  Valsalva,  750 

Skin,  hyperesthesia  of,  43 

in  broncho-pneumonia,  422 

in  lobar  pneumonia,  404 

in  tuberculosis,  325 

lesions  in  blastomycosis,  385 
Skoda's  veiled  puff,  284 
Slag  dust,  437,  441 
Sneezing,  diaphragm  and,  583 
Sound,  absorption  of,  59 

analysis,  57 

cracked  pot,  69 

diffusion,  59 

percussion,  63 

qualities,  57 

reflection,  59 

thoracic,  origin  of,  59 


Spasm  of  diaphragm,  583 

tonic,  of  diaphragm,  583 
Spes  phthisica,  326 
Sphygmograph,  165 
Sphygmomanometer  in  arterio-sclerosis, 

728 
Spine,  curvature  of,  30,  39 
Spirometer,  25 

Spleen,  percussion  dulness,  96 
Sporotrichosis,  pulmonary,  390 
diagnosis,  391 
etiology,  390 
morbid  anatomy,  390 
symptoms,  391 
Sputum  in  bronchiectasis,  282 

examination  of,  in  tuberculosis,  353 
in  lobar  pneumonia,  403 
in  malignant  disease  of  lungs,  505 
in  pulmonary  abscess,  463 
Stenosis,  aortic,  681 
mitral,  667 
pulmonary,  695 
tricuspid,  689 
Stethoscope,  107 
Streptothricosis,  pulmonary,  381 
cutaneous  test  for,  381 
diagnosis,  381 
etiology,  379 
morbid  anatomy,  379 
physical  signs,  380 
sputum  in,  381 
symptoms,  380 
Streptothrix,  354 
Subclavian  murmurs,  246,  342 
Subcutaneous  tuberculin  test,  355 
Subdiaphragmatic  abscess,  596 
abdominal  signs,  599 
diagnosis,  601 
etiology,  597 
gas-containing,  597,  600 

signs  in,  600 
morbid  anatomy,  598 
physical  signs,  599 
simple,  597 
thoracic  signs,  599 
inflammation,  597 
pyopneumothorax,  597,  600 
Subphrenic  abscess,  596 

peritonitis,  596 
Substernal  sounds,  215 
Succussion  splash,  128,  248 
in  pneumothorax,  574 


INDEX 


779 


Sympathetic  nerves  in  aneurism,  741 
Syphilis,  bronchiectasis  and,  278 
chronic  aortitis  and,  723 

endocarditis  and,  655 
myocardial  changes  in,  636 
myocarditis  and,  627 
of  bronchi,  491 
of  larynx,  490 
of  lungs,  492 

acquired,  493 

catarrh  and,  464 

congenital,  493 

diagnosis,  497 

fibroid  induration  in,  493 

gummata  in,  493 

morbid  anatomy,  492 

physical  signs,  495 

symptoms,  494 

tuberculosis  and,  497 

types,  496 
of  respiratory  tract,  490 
of  trachea,  491 
Syphilitic  aortitis,  718 

myocarditis  and,  629 
Systolic  murmur  in  aortic  insufficiency, 
680 

in  aortitis,  730 

in  mitral  stenosis,  674 

pulmonary,  667 
retraction  of  interspaces,  614 

Tachycardia,  156 
'  hypertrophy  of  heart  in,  623 

paroxysmal,  172,  190 
Teleoroentgenography,  622 
Temperature  in  tuberculosis,  317 

inverted,  321 
Terminal  pneumonia,  409 
Thoracentesis,  hemorrhagic  effusion  and, 

559 
Thoracic  aorta,  aneurism  of,  731 
Threshing  fever,  437 
Thrill,  198 

in  aneurism,  746 

presystolic,  672 

systolic,  in  aortic  stenosis,  684 
Thymic  tracheostenosis,  512 
Thymus,  75 

enlarged,  512 

adenoids  and,  513 
diagnosis,  517 
etiology,  513 


Thymus,  enlarged,  goitre  and,  513,  517 

Kopp's  asthma  and,  514 

morbid  anatomy,  513 

physical  signs,  515 

symptoms,  514 
evolution  of,  512 
function  of,  513 
murmurs  due  to,  247 
position,  136,  137,  138 
Thyroid  gland  in  tuberculosis,  332 
Toes,  clubbing  of,  519 
Tonsillitis,  chronic  endocarditis  and,  654 

endocarditis  and,  641 
Trachea  in  aneurism,  742 
syphilis  of,  491 

diagnosis,  492 

morbid  anatomy,  491 

physical  signs,  492 

symptoms,  491 
Tracheal  tugging  in  aneurism,  747 
Tracings,  sphygmographic,  164 
Traube's  double  sound,  244,  680 

semilunar  space,  95,  98 
Trauma,  pneumonia  and,  393 
Trichiniasis,  diaphragm  and,  591 

pulmonary  symptoms,  591 
Tricuspid  insufficiency,  685  ; 

diagnosis,  689 

morbid  anatomy,  686 

murmur  of,  232 

organic,  685 

pathologic  physiology,  686 

physical  signs,  687 

pulsation  of  jugulars  in,  687 

relative,  685 

symptoms,  687 
stenosis,  689 

diagnosis,  693 
..  -     etiology,  689 

morbid  anatomy,  690 

murmur  of,  234 

pathologic  physiology,  690 

physical  signs,  693 

polycythemia  in,  693 

symptoms,  693 
Tubercle  bacillus,  virulence  of,  295 
Tuberculosis,  miliary,  368 

endocarditis  and,  650 

etiology,  368 

malignant  endocarditis  and,  375 

meningeal  form,  376 

morbid  anatomy,  370 


780 


INDEX 


Tuberculosis,   miliary,  pulmonary  form, 

375 
symptoms,  371 
typhoid  fever  and,  375 

form,  374 
of  lungs,  293 

abscess  of  lung  and^  466 
acute,  361 

colds  and,  315 
anemia  in,  324 

aneurism  of  aorta  and,  739,  752 
arrested,  diagnosis,  352 
arthritis  in,  327 
auscultation  in,  339 
blood  pressure  in,  325 
blood-streaked  sputum  in,  313 
bronchiectasis  and,  278,  284,  310 
cardiac  phenomena  in,  342 
cardio-respiratory      murmurs,      247, 

342 
cardio-vascular  symptoms,  325 
cavity  in,  signs  of,  348 
chills  in,  324 
chronic,  293 

diseases  and,  298 

in  children,  physical  signs,  358 
symptoms,  358 

in  early  life,  357 
clubbing  of  fingers  in,  332 
coal  miners',  435 
cog-wheel  breathing  in,  340 
constitutional  symptoms,  317 
cough  in,  327 
deformity  of  chest  in,  310 
dextrocardia  in,  592,  596 
diagnosis,  352 
diaphragm  in,  592,  596 
diarrhea  in,  325 
diazo  reaction  in,  326 
distomatosis,  pulmonary,  and,  489 
dysphagia  in,  330 
dyspnea  in,  330 
etiology,  293 

examination  of  sputum  in,  353 
expectoration  in,  327 
feeble  breathing  in,  340 
fever  in,  317 
fibroid,  367 
fistula  in  ano  and,  315 
Florida,  361 

foreign   bodies  in  air-passages  and, 
291 


Tuberculosis    of   lungs,    gastro-intestinal 
symptoms,  316,  324 

tract  in,  311 
gold  miners',  436,  441 
granular  breathing  in,  340 
heart  in,  310 

disease  and,  343 
hemoptysis  in,  313,  328 
hemorrhagic  effusion  in,  557 
heredity  and,  295 
herpes  zoster  in,  326 
history,  312 
hoarseness  in,  315,  329 

hydatid  disease  and,  487 
hyperesthesia  in,  326 
Indian  and,  295 
infection  by  inhalation,  294 

by  ingestion,  294 

localized,  294 

of  fetus,  294 
influence  of  age  in,  299 
insanitary  surroundings  and,  296 
inspection  in,  231 
intrathoracic  tumors  and,  509 
iodide  of  potassium  in,  355 
ischio-rectal  abscess  and,  315 

fossa  in,  311 
jaundice  in,  325 
kidneys  in,  312 
Kronig's  isthmus  in,  337 
larynx  in,  311 

location  of  primary  focus,  306 
loculated  empyema  and,  556 
loss  of  weight  in,  323 
Louis'  law  in,  317 
malaise  in,  323 
malaria  and,  317 

malignant  disease  of  lungs  and,  509 
marital  infection  in,  294 
meninges  in,  312 

menstrual  function  in,  316,  319,  327 
mensuration  in,  335 
mental  attitude  in,  326 
mitral  stenosis  and,  672,  676 
morbid  anatomy,  299 
negro  and,  285 
nervous  system  in,  326 
neurasthenia  and,  323 
night  sweats  in,  324 
occupation  and,  297 
onset  of,  abrupt,  313 
insidious,  315 


INDEX 


781 


Tuberculosis  of  lungs,  pain  in,  329 
palpation  in,  334 
percussion  in,  337 
physical  signs,  118,  330 
pleural  space  in,  309 
pleurisy  in,  315,  527 
pneumoconiosis  and,  438 
pneumothorax  in,  568,  577 
pregnancy  and,  298 
prolonged  expiration  in,  340 
puerperal  period  and,  298 
pulmonary  infarction  and,  474 
purpura  in,  325 
rales  in,  342 
reinfection  in,  296 
resistance  to,  295 
rigidity  of  muscles  in,  334 
second  stage,  343 
skin  in,  325 
symptoms,  312 

subjective,  327 
syphilis  of  lungs  and,  497 
third  stage,  345 

physical  signs,  345 
thyroid  gland  in,  332 
typhoid  fever  and,  316 
urine  in,  326 
virulence  of,  295 
vocal  resonance  in,  342 
wavy  breathing  in,  340 
white  races  and,  295 
whooping  cough  and,  270 
Williams'  diaphragmatic  sign  in,  339 
with  retraction,  219 
X-ray  diagnosis,  356 
of  tracheo-bronchial  lymph  nodes,  360 

diagnosis,  361 

physical  signs,  360 

symptoms,  360 
Tuberculin  tests,  355 
conjunctival,  355 
cutaneous,  355 
Moro,  355 
percutaneous,  355 
von  Pirquet,  355 
subcutaneous,  355 
Tuberculous  broncho-pneumonia,  361,  426 
meningitis,  376 
etiology,  326 
morbid  anatomy,  376 
symptoms,  377 
pericarditis,  603,  606 


Tuberculous  pneumonia,  322,  366,  412 
Tumor,  intrathoracic,  474,  484,  498 
Tympany,  63 
bell,  69 
modified,  68 
Typhoid    fever,    acute    bronchitis    and, 
259 
lobar  pneumonia  and,  414 
malignant  endocarditis  and,  650 
miliary  tuberculosis  and,  375 
myocarditis  in,  627 
tuberculosis  and,  316 
form  of  endocarditis,  649 

of  miliary  tuberculosis,  374 
pneumonia,  409 

Ulcerative  endocarditis,  644 
Urine  in  broncho-pneumonia,  423 

in  lobar  pneumonia,  404 

in  tuberculosis,  326 
Urticaria,  bronchial  asthma  and,  275 
Uskoff,  sphygmotonograph,  161 

Valve  areas  in  chest  wall,  211 
Valves  of  heart,  position,  152 
Valvular  disease  of  heart,  654 
hypertrophy  in,  622 
pathological  physiology,  656 
lesions,  combined,  656 
Vasomotor  test,  Crampton's,  177 
Veiled  puff  of  Skoda,  284 
Veins,  aneurism  of  aorta  and,  743 
jugular,  pulsation  in,  687 
murmurs  in,  247 

pulmonary,  hydrothorax  and,  566 
Vena     cava,     aneurism     of    aorta    and, 
743 
inferior,  238 

rupture  of  aneurism  into,  756 
superior,  238 
Ventricular  septum.,  imperforate,  702 
Vesicular  sounds,  111 
Vibrations,  rhythmic,  53 
sympathetic,  54 
unrhythmic,  54 
Vocal  fremitus,  45 
vibrations  of,  47 
resonance,  130 
in  children,  140 
Voice  production,  mechanism,  46 

sounds,  130 
von  Pirquet  tuberculin  test,  355 


782  index 

Wandering  pneumonia,  410  Whooping  cough,  symptoms,  268 
Water-hammer  pulse,  679  tuberculosis  and,  270 

Weight,  loss  of,  in  tuberculosis,  323  Williams'  diaphragmatic  sign,  596 
Whispered  sounds,  132  in  tuberculosis,  339,  596 

Whooping  cough,  267  Wounds,  gunshot,  of  chest,  559 
acute  bronchitis  and,  259 

broncho-pneumonia  and,  270  X-ray  diagnosis  of  tuberculosis,  356 
diagnosis,  270  examination  in  aneurism  of  aorta,  749 

etiology,  267  in  children,  147 

measles  and,  270  in  lobar  pneumonia,  411 

morbid  anatomy,  267 

physical  signs,  269  Zt-ckergussherz,  615 


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definition  that  defines  in  the  fewest  possible  words. 

Howard  A.  Kelly,  M.  D.,  Johns  Hopkins  University,  Baltimore. 

"  The  American  Illustrated  Dictionary  is  admirable.  It  is  so  well  gotten  up  and  of  such 
convenient  size.     No  errors  have  been  found  in  my  use  of  it." 

Owen's  Treatment  of  Emergencies 

The  Treatment  of  Emergencies.  By  Hubley  R.  Owen,  M.  D., 
Surgeon  to  the  Philadelphia  General  Hospital.  i2mo  of  350  pages, 
with  249  illustrations.  Just  Issued. 

Dr.  Owen's  book  is  a  complete  treatment  of  emergencies.  It  gives  you  not 
only  the  actual  technic  of  the  procedures,  but,  what  is  equally  important,  the  un- 
derlying principles  of  the  treatments,  and  the  reason  why  a  particular  method  is 
advised.  You  get  treatments  of  fractures,  of  contusions,  of  wounds.  Particularly 
strong  is  the  chapter  on  gun-shot  wounds,  which  gives  the  new  treatments  that  the 
great  European  War  has  developed.  You  get  the  principles  of  hemorrhage,  to- 
gether with  its  constitutional  and  local  treatments.  You  get  chapters  on  sprains, 
strains,  dislocations,  burns,  sunburn,  chilblain,  asphyxiation,  convulsions,  hysteria, 
apoplexy,  exhaustion,  opium  poisoning,  uremia,  electric  shock,  bandages,  and 
a  complete  discussion  of  artificial  respiration,   including  mechanical  devices. 


LEGAL   MEDICINE 


Bohm  and  Painter's  Massage 

Massage.  By  Max  Bohm,  M.  D.,  of  Berlin,  Germany.  Edited,  with  an 
Introduction,  by  Charles  F.  Painter,  M,  D.,  Professor  of  Orthopedic  Sur- 
gery at  Tufts  College  Medical  School,  Boston.  Octavo  of  91  pages,  with  97 
practical  illustrations.  Cloth,  $1.75  net. 

Draper's  Legal  Medicine 

A  Text-Book  of  Legal  Medicine.  By  Frank  Winthrop  Draper,  A.  M., 
M.  D.,  Late  Professor  of  Legal  Medicine  in  Harvard  University,  Boston. 
Octavo  of  573  pages,  illustrated.     Cloth, .$4.00  net ;  Half  Morocco,  $5.50  net, 

Golebiewski  and  Bailey's  Accident  Diseases 

Atlas  and  Epitome  of  Diseases  Caused  by  Accidents.      By   Dr.  Ed. 

Golebiewski,  of  Berlin.  Edited,  with  additions,  by  Pearce  Bailey,  M.  D., 
Consulting  Neurologist  to  St.  Luke's  Hospital,  New  York.  With  71  colored 
illustrations  on  40  plates,  143  text  illustrations,  and  549  pages  of  text.  Cloth, 
$4.00  net.     In  Saunders  Hand- Atlas  Series. 

Hofmann  and   Peterson's   Legal   Medicine      Hand-Atiies 

Atlas  of  Legal  Medicine.  By  Dr.  E.  von  Hofmann,  of  Vienna. 
Edited  by  Frederick  Peterson,  M.  D.,  Professor  of  Psychiatry  in  the 
College  of  Physicians  and  Surgeons,  New  York.  With  1 20  colored  figures 
on  56  plates  and  193  half-tone  illustrations.      Cloth,  $3.50  net. 

Jakob  and  Fisher's  Nervous  System  sTtuS 

Atlas  and   Epitome  of  the  Nervous   System  and  its   Diseases.      By 

Professor  Dr.  Chr.  Jakob,  of  Erlangen.  Edited,  with  additions,  by  Ed- 
ward D.  Fisher,  M.  D.,  University  and  Bellevue  Hospital  Medical  College. 
With  83  plates  and  copious  text.     Cloth,  $3. 50  net. 

Spear's  Nervous  Diseases  Just  out 

A  Manual  of  Nervous  Diseases.  By  Irving  J.  Spear,  M.  D,.  Professor 
of  Neurology  at  the  University  of  Maryland,  Baltimore.  i2mo  of  660  pages, 
illustrated.  Cloth,  $2.75  net. 

This  is  a  comprehensive  digest,  supplying  the  means  to  a  clear  understanding  of 
neurology,  and  robbing  that  subject  of  much  of  its  difficulty.  You  are  given,  first, 
a  brief  description  of  the  practical  anatomy  and  physiology,  with  those  facts  and 
theories  that  bear  on  the  mechanism  of  organic  nervous  diseases.  Then  pathology 
is  given,  the  simpler  diseases  being  considered  first,  gradually  preparing  the  reader 
to  grasp  the  more  difficult  ones.  The  descriptions  are  clear  and  brief,  differential 
diagnoses  and  treatments  being  brought  out  very  definitely.  Only  the  most  recent 
accepted  facts  have  been  considered.  For  the  treatments  recommended,  no  special 
apparatus  is  required  beyond  a  galvanic  and  faradic  battery;  they  demand  no 
special  training,  and  they  are  easily  remembered. 


SAUNDERS'  BOOKS  ON  CHILDREN. 


American  Pocket  Dictionary  New  (9th)  Edition 

American  Pocket  Medical  Dictionary.  Edited  by  W.  A.  New- 
man  Dorland,  M.  D. ,  Editor  "American  Illustrated  Medical  Dic- 
tionary." Containing  the  pronunciation  and  definition  of  the  principal 
words  used  in  medicine  and  kindred  sciences,  with  75  extensive  tables. 
With  693  pages.  Flexible  leather,  with  gold  edges,  $1.25  net;  with 
patent  thumb  index,  #1.50  net. 

"  I  can  recommend  it  to  our  students  without  reserve." — J.  H.  HOLLAND,  M.  D.,  Dean 
of  the  Jefferson  Medical  College,  Philadelphia. 

Morrow's  Immediate  Care  of  Injured  Second  Edition 

Immediate  Care  of  the  Injured.  By  Albert  S.  Morrow,  M.  D., 
Adjunct  Professor  of  Surgery  at  the  New  York  Polyclinic.  Octavo  of  360 
pages,  with  242  illustrations.      Cloth,  $2.50  net. 

Dr.  Morrow's  book  on  emergency  procedures  is  written  in  a  definite  and  decisive  style, 
the  reader  being  told  just  what  to  do  in  every  emergency.  It  is  a  practicad  book  for  every 
day  use,  and  the  large  number  of  excellent  illustrations  can  not  but  make  the  treatment  to 
be  pursued  in  any  case  clear  and  intelligible.    Physicians  and  nurses  will  find  it  indispensible. 

Powell's    Diseases    Of   Children  Third  Edition,  Revised 

Essentials  of  the  Diseases  of  Children.  By  William  M.  Powell, 
M.  D.  Revised  by  Alfred  Hand,  Jr.,  A.  B.,  M.  D.,  Dispensary 
Physician  and  Pathologist  to  the  Children's  Hospital,  Philadelphia. 
i2mo  volume  of  259  pages.  Cloth,  $1.25  net.  In  Saunders1 
Question-  Compend  Series. 

Shaw  on  Nervous  Diseases  and  Insanity        Fifth  edition 

Essentials  of  Nervous  Diseases  and  Insanity  :  Their  Symptoms 
and  Treatment.  A  Manual  for  Students  and  Practitioners.  By  the  late 
John  C.  Shaw,  M.  D.,  Clinical  Professor  of  Diseases  of  the  Mind  and 
Nervous  System,  Long  Island  College  Hospital,  New  York.  i2mo  of 
204  pages,  illustrated.  Cloth,  $1.25  net.  In  Saunders''  Question- Com- 
pend Series. 

"  Clearly  and  intelligently  written ;  we  have  noted  few  inaccuracies  and  several  sug- 
gestive points.  Some  affections  unmentioned  in  many  of  the  large  text-books  are  noted.' 
— Boston  Medical  and  Surgical  Journal. 

Brady's  Personal  Health  just  out 

Personal  Health:  A  Doctor  Book  for  Discriminating  People.  By 
William  Brady,  M.D.,  Elmira,  N.Y.  i2mo  of  406  pages.  Cloth,  $1.50  net 

Hecker,  Trumpp,  and  Abt  on  Children 

Atlas  and  Epitome  of  Diseases  of  Children.  By  Dr.  R.  Hecker 
and  Dr.  J.  Trumpp,  of  Munich.  Edited,  with  additions,  by  Isaac  A. 
Abt,  M.D.,  Assistant  Professor  of  Diseases  of  Children,  Rush  Medical 
College,  Chicago.  With  48  colored  plates,  144  text-cuts,  and  453  pages 
of  text.     Cloth,  $5.00  net. 

The  many  excellent  lithographic  plates  represent  cases  seen  in  the  authors'  clinics,  and 
have  been  selected  with  great  care,  keeping  constantly  in  mind  the  practical  needs  of  the 
general  practitioner.  These  beautiful  pictures  are  so  true  to  nature  that  their  study  is 
equivalent  to  actual  clinical  observation.  The  editor,  Dr.  Isaac  A.  Abt,  has  added  all  new 
methods  of  treatment. 


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